2009年3月31日星期二
治癌奇方[一]
主治：各种癌/瘤 配方：生五灵脂１０克，生黑牵牛２０克，生香附子１０克，生广木香１０克． 用法：买药时加工成粉，加白醋调糊为丸，阴干．一次１０克．生姜汁送服，每天３－４次（小儿药量减半）．也可以不调糊，服药时加些醋． 注意：不得吃人参。孕妇不可用。 说明：一般病例３０分钟见效，经千余例临验，疗效100%，被称为神方！ 本方前三味药是祖传秘方，第四味药是贡献人研究所加． 献方人：广东饶平县三饶镇西巷头民间医师 李清岩 公开祖传秘方，救死扶伤，功德无量！ 经济困难的同修在给人治病时可以适当收取成本以维生，但绝不能牟取暴利！ 任何人不得私作主张修改药方，那会害死人！若遭天谴，后果自负! 请广泛转贴，举手之劳，可以解救病苦众生，必得善报
2009年1月17日星期六
贲门癌放射治疗方法
贲门癌占胃癌的53.3%，以腺癌为主。传统认为腺癌对放射线不敏感，经近年来的研究，对放射治疗贲门癌有了新的认识。据报道贲门癌术前放疗DT 40 Gy可提高手术切除率，降低淋巴结转移阳性率，明显提高1、3年生存率。单纯放射治疗贲门癌，可以取得与扩大根治术相同的效果，认为放射治疗局部作用强，可以有效抑制和杀死癌细胞。而锎252能自发裂变发射中子射线，中子属于高LET（线性能量传递）射线，其具有相对生物效应（RBE）高；氧增效比（OER）低；没有或很少有亚致死性损伤修复及潜在性致死损伤修复；并且对各时相癌细胞敏感性均较高；对肿瘤内的乏氧细胞能够很好地杀灭。并且中子对腺癌也有很好的生物学效应。
贲门癌治疗失败的主要原因为腹腔内外淋巴结转移，其次为局部未控。UFTM方案所用的药物优福定属周期特异性药物，优福定是5-FU的衍生物喃呋啶与非化疗药物脲嘧啶的混合物。丝裂霉素属周期非特异性药物。代培水等［7］报道晚期贲门癌放射治疗加喃呋啶静点较单纯放射治疗可明显提高 1 年生存率。采用放疗加UFTM方案治疗后，患者吞咽改善率达100%，X线好转率达84.7%，1年生存率为82.1%，与行扩大根治术具有相似的效果，并优于单纯化疗者。说明UFTM方案一方面可以增加肿瘤放疗的敏感性，同时可以消灭有可能出现的癌转移。以往认为：粘液腺癌及印戒细胞癌对放疗无效，故为禁忌。我们观察了6例经病理证实的患者，从治疗情况看，对中子射线还是敏感的。治疗后的效果是满意的，说明粘液腺癌及印戒细胞癌对中子射线是敏感的。
UFTM方案毒副作用小，血象下降及胃肠道反应经对症处理可在短期内恢复，不影响治疗，且方法简单易于推广。与内、外放疗相伴，不仅可改善近期疗效，且可提高1年生存率。3、5年生存率有待我们进一步的跟踪观察。研究结果表明，锎中子近距离加外照射放疗结合化疗的综合治疗手段是治疗晚期贲门癌的有效方法。
贲门癌治疗失败的主要原因为腹腔内外淋巴结转移，其次为局部未控。UFTM方案所用的药物优福定属周期特异性药物，优福定是5-FU的衍生物喃呋啶与非化疗药物脲嘧啶的混合物。丝裂霉素属周期非特异性药物。代培水等［7］报道晚期贲门癌放射治疗加喃呋啶静点较单纯放射治疗可明显提高 1 年生存率。采用放疗加UFTM方案治疗后，患者吞咽改善率达100%，X线好转率达84.7%，1年生存率为82.1%，与行扩大根治术具有相似的效果，并优于单纯化疗者。说明UFTM方案一方面可以增加肿瘤放疗的敏感性，同时可以消灭有可能出现的癌转移。以往认为：粘液腺癌及印戒细胞癌对放疗无效，故为禁忌。我们观察了6例经病理证实的患者，从治疗情况看，对中子射线还是敏感的。治疗后的效果是满意的，说明粘液腺癌及印戒细胞癌对中子射线是敏感的。
UFTM方案毒副作用小，血象下降及胃肠道反应经对症处理可在短期内恢复，不影响治疗，且方法简单易于推广。与内、外放疗相伴，不仅可改善近期疗效，且可提高1年生存率。3、5年生存率有待我们进一步的跟踪观察。研究结果表明，锎中子近距离加外照射放疗结合化疗的综合治疗手段是治疗晚期贲门癌的有效方法。
胃底贲门癌
根据日本“外科、病理胃癌处理规约”，将胃大弯和胃小弯各作三等分，分别连接各对应点，则其中最上部分即为贲门胃底部，发生于该处的恶性肿瘤称为贲门胃底癌，其也属于胃癌的范畴之内。
病因：与其它肿瘤一样，病因不详，可能与饮食因素、环境因素、遗传因素以及幽门螺杆菌感染有关。另外存在诸如慢性萎缩性胃炎、胃溃疡、胃息肉、胃粘膜上皮细胞化生及胃粘膜上皮异型增生等癌前变化。
临床表现：病变早期无明显症状，即使有一些上消化道症状，也属非特异性，常导致延误诊断，故40岁以上成人如无诱因出现上消化道症状或原有症状加重变化以及出现原因不明的黑便和大便隐血阳性，特别是具有家族史时，应进一步诊断以排除恶性肿瘤可能；发展至进展期时则可出现如进行性吞咽困难，上腹部肿物以及锁骨上淋巴结肿大等较特异性的症状。
诊断：早期贲门胃底癌的诊断较困难，较易漏诊，至进展期则诊断相对较易。密切结合临床体检、X线钡餐造影检查以及胃镜结合病理学检查常可确诊。
治疗：早期病变的治疗推荐采用手术治疗；进展期病变的治疗方法多样，如放、化疗，热疗，手术治疗乃至晚期的姑息性治疗及中医中药的治疗等。手术根治包括病灶及其周围正常组织的切除，局部淋巴结（如贲门左右、胃大小弯侧及腹主动脉旁淋巴结等）清扫，由于贲门胃底癌的位置，根据肿瘤大小及侵犯范围常决定行近端胃大部切除术或全胃切除+空肠代胃术。由于贲门胃底癌的特殊性，食管腹段长度的限制，手术视野的暴露情况，以及术中处理的难易，常将贲门胃底癌的手术治疗归于胸外科范畴，经胸腔经膈肌行根治术或经胸腹联合切口行根治术。
病因：与其它肿瘤一样，病因不详，可能与饮食因素、环境因素、遗传因素以及幽门螺杆菌感染有关。另外存在诸如慢性萎缩性胃炎、胃溃疡、胃息肉、胃粘膜上皮细胞化生及胃粘膜上皮异型增生等癌前变化。
临床表现：病变早期无明显症状，即使有一些上消化道症状，也属非特异性，常导致延误诊断，故40岁以上成人如无诱因出现上消化道症状或原有症状加重变化以及出现原因不明的黑便和大便隐血阳性，特别是具有家族史时，应进一步诊断以排除恶性肿瘤可能；发展至进展期时则可出现如进行性吞咽困难，上腹部肿物以及锁骨上淋巴结肿大等较特异性的症状。
诊断：早期贲门胃底癌的诊断较困难，较易漏诊，至进展期则诊断相对较易。密切结合临床体检、X线钡餐造影检查以及胃镜结合病理学检查常可确诊。
治疗：早期病变的治疗推荐采用手术治疗；进展期病变的治疗方法多样，如放、化疗，热疗，手术治疗乃至晚期的姑息性治疗及中医中药的治疗等。手术根治包括病灶及其周围正常组织的切除，局部淋巴结（如贲门左右、胃大小弯侧及腹主动脉旁淋巴结等）清扫，由于贲门胃底癌的位置，根据肿瘤大小及侵犯范围常决定行近端胃大部切除术或全胃切除+空肠代胃术。由于贲门胃底癌的特殊性，食管腹段长度的限制，手术视野的暴露情况，以及术中处理的难易，常将贲门胃底癌的手术治疗归于胸外科范畴，经胸腔经膈肌行根治术或经胸腹联合切口行根治术。
食管癌及贲门癌诊断
诊断
（一）病史
（二）X线食管钡餐造影：是诊断中晚期食管癌的主要方法。可见食管粘膜纹中断，紊乱，管腔不同程度的狭窄，充盈缺损、龛影、管壁扩张受限、僵直等。早期病变可无阳性发现。
（三）食管拉网细胞学检查：食管拉网细胞学检查的阳性率为90%，这种方法操作简便，痛苦少，在防癌普查中尤为有用。
（四）纤维食管镜检查：这是诊断食管癌比较可靠的方法，但由于早期食管癌位于粘膜层比较小，内窥镜容易遗漏，如果检查时在食管腔内注入甲苯胺蓝或碘溶液染色则有助于早期癌的发现。纤维食管镜检查时，可同时做腔内粘液涂片和取活体组织检查。
五、鉴别诊断
（一）食管良性肿瘤
（二）贲门痉挛
（三）食管疤痕狭窄
（一）病史
（二）X线食管钡餐造影：是诊断中晚期食管癌的主要方法。可见食管粘膜纹中断，紊乱，管腔不同程度的狭窄，充盈缺损、龛影、管壁扩张受限、僵直等。早期病变可无阳性发现。
（三）食管拉网细胞学检查：食管拉网细胞学检查的阳性率为90%，这种方法操作简便，痛苦少，在防癌普查中尤为有用。
（四）纤维食管镜检查：这是诊断食管癌比较可靠的方法，但由于早期食管癌位于粘膜层比较小，内窥镜容易遗漏，如果检查时在食管腔内注入甲苯胺蓝或碘溶液染色则有助于早期癌的发现。纤维食管镜检查时，可同时做腔内粘液涂片和取活体组织检查。
五、鉴别诊断
（一）食管良性肿瘤
（二）贲门痉挛
（三）食管疤痕狭窄
贲门癌传染吗
在过去的几百多年中，癌会不会传染的问题经常被提出来，并进行了不断的观察研究。尤其从1908年发现了病毒可以引起肿瘤之后，这个问题更加引人注目了。 从一般概念讲，病毒是有传染性的，但各种病毒的传染力强弱不同。病毒感染后，临床发病的人只不过1%～1‰，而更多的人并不发病，处于隐性感染状态。病毒感染后是否发病，和机体的防御机能有重要关系。机体防御机能强，即使有病毒感染，也可能终身不发生疾病。 现巳确定，有一百多种病毒可引起动物的三十多种肿瘤。有些病毒还能引起人类肿瘤。这样，从客观上就存在着肿瘤可能传染的物质基础。在人的伯基特氏淋巴瘤、鼻咽癌、乳腺癌、白血病、宫颈癌、黑色素瘤内，也发现了病毒或这类病毒颗粒。
不仅如此，在动物实验方面，有人将患有滤过性肉瘤鸡的脾脏血，注射到健康鸡的身上，结果健康鸡也得了滤过性肉瘤。还有人让吸过患乳腺癌小鼠血的跳蚤，再咬健康的小鼠，果然成功地把肿瘤接种在健康的小鼠身上。但是这种实验至今在人的身上并没有得到同样的证实。而且即使在动物身上，与患癌动物居住在一起的健康动物，也没有发现它们被直接传染上癌症。 国外医学家对肿瘤疗养院内的患者进行了长期观察，发现伴有溃疡的癌症患者，与没有溃疡的癌症患者，长时间地相处在一起，在他们之间从来没有出现过互相传染。另一方面，经医生治疗的癌症患者数不胜数，而医生的癌症患病率并不比一般人为高。 目前普遍存在的大量事实是，患癌的动物和健康的动物同住一室，并没有发现直接传染的例子。在医院里不同种类癌病人长期同居一室，多少年来，从未发现过互相传染。
医务人员长期接触癌病人，并没有发现他们比一般人的癌发病率增高。这些事实说明，一般肿瘤没有传染性，同肿瘤病人的一般接触，是不会被传染的。所以，直到今天，所有医院对于肿瘤病人并不采取隔离制度。
不仅如此，在动物实验方面，有人将患有滤过性肉瘤鸡的脾脏血，注射到健康鸡的身上，结果健康鸡也得了滤过性肉瘤。还有人让吸过患乳腺癌小鼠血的跳蚤，再咬健康的小鼠，果然成功地把肿瘤接种在健康的小鼠身上。但是这种实验至今在人的身上并没有得到同样的证实。而且即使在动物身上，与患癌动物居住在一起的健康动物，也没有发现它们被直接传染上癌症。 国外医学家对肿瘤疗养院内的患者进行了长期观察，发现伴有溃疡的癌症患者，与没有溃疡的癌症患者，长时间地相处在一起，在他们之间从来没有出现过互相传染。另一方面，经医生治疗的癌症患者数不胜数，而医生的癌症患病率并不比一般人为高。 目前普遍存在的大量事实是，患癌的动物和健康的动物同住一室，并没有发现直接传染的例子。在医院里不同种类癌病人长期同居一室，多少年来，从未发现过互相传染。
医务人员长期接触癌病人，并没有发现他们比一般人的癌发病率增高。这些事实说明，一般肿瘤没有传染性，同肿瘤病人的一般接触，是不会被传染的。所以，直到今天，所有医院对于肿瘤病人并不采取隔离制度。
不同手术径路治疗贲门癌的对比研究
不同手术径路治疗贲门癌的对比研究 （北京）为了探讨经胸、经腹手术径路行贲门癌切除术的优缺点及选择原则。研究者将160例贲门癌患者分为经腹切口、经左胸切口组，每组80例，行贲门癌手术治疗，比较两组的平均淋巴结清扫数、切缘癌残留率、手术根治率、围手术期病死率、术后并发症发生率、术后平均恢复时间、生存率。结果经腹切口组和经左胸切口组的平均淋巴结清除个数分别为15.7和10.6个，上切缘癌残留率分别为5.0%和1.2%，两组比较差异均有统计学意义；下切缘癌残留率、围手术期病死率、手术根治率、并发症发生率、手术后平均恢复时间、生存率分别为1.2%，0.0%，81.2%，10.0%，10d，53.7%和1.2%，1.2%，83.7%，11.2%，12d，56.2%，两组比较差异均无统计学意义。可见两种手术切口各有其优缺点，手术切口的选择应重点考虑病变的部位和范围以及患者的身体状况。
贲门癌的外科治疗近远期疗效
贲门癌的外科治疗近远期疗效
贲门癌的手术疗效比食管癌要差。国内三大组切除率73.7%～82.1%，切除死亡率1.7%～2.4%。三大组的5年生存率19.0%～24.0%，10年生存率8.6%～14.3%。
影响贲门癌远期生存的主要因素为淋巴结有无转移，肿瘤是否浸润浆膜以及切除性质（根治或姑息）。贲门癌的国际TNM分期，由于综合了前两个可变因素，同样是预测病人转归的有效指标。
（四）残胃贲门癌
远侧胃部分切除术后残胃囊发生癌的报告日益增多。其发生率为0.55%～8.9%，其中发生在贲门部的占全部的16.4%～58.5%，残胃贲门癌在贲门癌中的发生率为1.5%～2.7%。
残胃癌的定义：
1.首次胃次全切除是治疗良性疾病，如胃或十二指肠溃疡。
2.距首次胃部分切除到发生癌瘤间隔期不少于5年。一般认为多发生于毕氏Ⅱ式术后，但也有持相反意见的。首次胃切除术后胃酸分泌减少，十二指肠液反流刺激，萎缩性胃炎及肠上皮化生的存在皆为可能的诱因。
贲门癌的手术疗效比食管癌要差。国内三大组切除率73.7%～82.1%，切除死亡率1.7%～2.4%。三大组的5年生存率19.0%～24.0%，10年生存率8.6%～14.3%。
影响贲门癌远期生存的主要因素为淋巴结有无转移，肿瘤是否浸润浆膜以及切除性质（根治或姑息）。贲门癌的国际TNM分期，由于综合了前两个可变因素，同样是预测病人转归的有效指标。
（四）残胃贲门癌
远侧胃部分切除术后残胃囊发生癌的报告日益增多。其发生率为0.55%～8.9%，其中发生在贲门部的占全部的16.4%～58.5%，残胃贲门癌在贲门癌中的发生率为1.5%～2.7%。
残胃癌的定义：
1.首次胃次全切除是治疗良性疾病，如胃或十二指肠溃疡。
2.距首次胃部分切除到发生癌瘤间隔期不少于5年。一般认为多发生于毕氏Ⅱ式术后，但也有持相反意见的。首次胃切除术后胃酸分泌减少，十二指肠液反流刺激，萎缩性胃炎及肠上皮化生的存在皆为可能的诱因。
贲门癌中医中药治疗
常用于贲门癌外科手术后或与化学治疗、放射治疗等合并应用。已证明在贲门癌的综合治疗中，中医和中药与其他疗法使用，可提高综合疗效，尤其在减少化疗对机体的不良反应、提高人体抵抗力及改善生活质量等方面具有一定的作用。
随着近年中医药现代化方面的进展，剂型方面有了改变，有冲剂、片剂，服用更为方便，还有了针剂，对已经不能口服的贲门癌病人来说，也可试用。此外，还有不少中西医结合的新的技术、新的方法可采用。以上这些，都可以根据晚期贲门癌病人的不同情况采用一种或多种方法，当然也可应用自己固有的综合方法治疗。中医处方的原则在晚期贲门癌的中医治疗中显得尤为重要，因为目前口服汤药还是最主要的治疗方式。晚期贲门癌的中医处方，大致都包含有三个组成部分。一个组成部分叫做“辨证论治”。依据中医理论，对贲门癌病人当时的情况：癌肿情况，全身情况，各个脏器的功能情况，以及脉象、舌象、体征等综合分析，按照病因、病机，据以组方。另一个组成部分，叫“辨病论治”，或者可以叫“辨癌论治”。那就是从中草药中，选择一些可能有抗癌作用的药物，放入方中。所谓可能有抗癌作用的药物，是指或者其中含有某种抗癌的成分；或者在动物实验中有一定的抗癌作用；或者过去中医传统用于抗癌或者民间习惯应用者。而所有这些，都没有在人体中得到证实。另一个组成部分，则是“对症治疗”的药物。胃癌常有疼痛，加一些止痛中药；有时有“黑粪”，加一些止血的中药；胃口不好，加一些开胃的药物；便闭或者腹泻，也可加相应的药物。
随着近年中医药现代化方面的进展，剂型方面有了改变，有冲剂、片剂，服用更为方便，还有了针剂，对已经不能口服的贲门癌病人来说，也可试用。此外，还有不少中西医结合的新的技术、新的方法可采用。以上这些，都可以根据晚期贲门癌病人的不同情况采用一种或多种方法，当然也可应用自己固有的综合方法治疗。中医处方的原则在晚期贲门癌的中医治疗中显得尤为重要，因为目前口服汤药还是最主要的治疗方式。晚期贲门癌的中医处方，大致都包含有三个组成部分。一个组成部分叫做“辨证论治”。依据中医理论，对贲门癌病人当时的情况：癌肿情况，全身情况，各个脏器的功能情况，以及脉象、舌象、体征等综合分析，按照病因、病机，据以组方。另一个组成部分，叫“辨病论治”，或者可以叫“辨癌论治”。那就是从中草药中，选择一些可能有抗癌作用的药物，放入方中。所谓可能有抗癌作用的药物，是指或者其中含有某种抗癌的成分；或者在动物实验中有一定的抗癌作用；或者过去中医传统用于抗癌或者民间习惯应用者。而所有这些，都没有在人体中得到证实。另一个组成部分，则是“对症治疗”的药物。胃癌常有疼痛，加一些止痛中药；有时有“黑粪”，加一些止血的中药；胃口不好，加一些开胃的药物；便闭或者腹泻，也可加相应的药物。
亲人贲门癌的手术治疗方法
（一）贲门癌的手术适应证
迄今为止，手术治疗是公认的贲门癌的首选治疗。由于其组织学为腺癌或粘液腺癌，放射治疗几乎无效，化学治疗效果也甚微。贲门癌手术适应证：①经X线、细胞学及内镜确诊；②超声检查、腹部CT扫描或腹腔镜检除外淋巴结、肝、肾上腺、网膜、腹膜及盆腔转移，无腹水；③一般情况中等以上，无重大心肺或其他脏器合并症。
由于贲门的解剖学特点，与肝、脾、横结肠、胰尾、肾、肾上腺、小肠、膈肌、后腹膜等诸多脏器相邻，又具有丰富的淋巴引流，向上入纵隔，向下沿大弯及小弯两条主要通道扩散，还可在胃壁内浸润，甚至达到全胃，因此一般的消化道造影不可能显示全部上述各个进程，应用发泡剂双重对比造影，可以清楚显示肿块、软组织影、粘膜破坏、溃疡、胃壁增厚的范围等，但X线改变常要比实际情况轻。应用腹部CT，可以了解肿物与周围器官之关系，但是比较食管的CT所见，贲门癌的阳性发现往往不太肯定，譬如是否侵及胰，往往判断不正确，CT怀疑有胰尾浸润而实际并无粘连，CT认为与胰无关联，但开腹肿瘤与胰浸润粘连成团。CT有助于发现肝转移，但对局部淋巴结转移的判断就不太准确。总之，在术前判断贲门癌之发展程度，估计其切除可能性等是一件相当困难的事，是临床到目前尚未解决的难题。为了不使病人失去治疗机会。腹部B超、CT以及食管胃造影等检查的阳性发现，除非确证已有广泛扩散转移，都应给予探查，争取切除病变并恢复消化道连续性。
（二）贲门癌的手术途径及方法
医科院肿瘤医院胸外科习惯采用左胸后外侧标准开胸切口，经第7肋床或肋间，然后在左膈顶部以食管为轴心作辐射状切口开腹。此种径路，对贲门区显露良好，足以行次全胃切除及胃周及胃左血管的淋巴结清扫。如需要扩大切除范围，行全胃或合并切除脾、部分胰等，则可将该切口向前下延到上腹壁，切断左肋软骨弓膈肌及腹壁肌肉，很方便地变成胸腹联合切口，充分显露上腹部。
在心肺功能储备低下和高龄病人中，可以采用颈腹二切口非开胸食管内翻拨脱部分胃切除，食管胃颈部吻合术。先开腹探查病变可以切除后，通过胃底或腹段食管开口将食管探条送到颈部，此时颈部食管已经显露，在准备作吻合部位之下方将食管结扎固定在探条上，切断上方食管，持续而均匀地牵拉探条，将食管自上而下翻转拔脱。游离胃常规切除部分胃，大弯剪裁成管状，经食管床上提入颈与食管吻合，这种手术的缺点是胃切除范围受限，可以导致胃侧切缘不净有残余癌。当纵隔过去有炎症，如淋巴结核而发生粘连时，会使翻转拔脱遇到困难，拔不动或是撕裂气管支气管膜部，发生后一种情况时需立即开胸修补，如事先已经估计拔脱有困难时，最好采用开胸切除的办法。
对心肺功能不足病人还有一种手术径路，就是联合胸骨正中切开和上腹正中切口，术中注意防止双侧胸膜破裂，并将心包自膈面游离，中线切开膈肌达食管裂孔，将心包前提显露后纵膈，然后常规将贲门癌及下段食管切除，残胃上提在后纵隔与食管吻合。此种切口显露后纵隔受一定限制，可以使用食管胃机械吻合器以保证吻合口质量。
常用的手术方法是近侧胃次全切除术。适应于贲门部肿瘤体积不大，沿小弯侵延不超过其全长的1/3时。手术具体操作如下：左后外第7肋床或肋间开胸，探查下段食管，然后以裂孔为轴心向左前切开膈肌、探腹，无肝、腹膜转移或广泛淋巴结转移时，沿大弯离断大网膜、左胃网膜动脉和胃脾韧带中的胃短动脉，离断左侧膈肌脚，完全显露下段食管，清除该部位（包括下肺韧带内）淋巴结。纱布垫开胰体及尾，显露胃左血管及其附近的淋巴结，仔细清扫淋巴结，结扎切断胃左血管，离断肝胃韧带，近侧胃完全游离，在大弯侧裁制胃管，如有胃缝合机可节省操作时间。要求切缘距肿瘤边不＜5cm。将胃管顺时针旋转90°，然后与食管下残端对端吻合，里层是全层结节缝合，外层将胃浆肌层向上套叠包绕吻合口约2cm，如望远镜状。吻合前为防止胃口粘膜过长，外翻覆盖肌层边影响吻合操作，可先环状切开胃管口部肌层，此时松弛的粘膜由于远侧肌层回缩而如袖状裸露。充分作粘膜下层止血，齐远侧肌层平面剪除多余之粘膜，此时胃管口的粘膜正好与肌层相平，吻合时视野十分清晰，有助于严密对合。
肿瘤浸润超过胃小弯长度一半时需行全胃切除，需离断全部5组胃的血供，全胃切除后缝合十二指肠端，作食管空肠吻合术。最简单的是食管空肠端侧吻合，空肠空肠侧侧吻合术，或者是Roux-Y食管空肠对端吻合，空肠空肠端侧吻合术。作者认为前者操作较简，空肠血运较后者保存更好。
如肿瘤已侵及胃脾韧带或胰尾，则可在次全或全胃切除同时行脾、胰尾切除术。注意妥善缝合胰的切断面，最好再用大网膜覆盖，以防止发生胰管瘘。
贲门癌手术治疗时胃切除范围一直是有争议的问题。有主张一律行全胃切除，有的作者主张整块切除全胃、脾、胰尾、网膜及区域淋巴结取得改进的生存。也有比较次全及全胃切除术后疗效，发现两者之存活率并无差别，建议仅在肿瘤累及胃体时作全胃切除。还有的作者发现在全胃切除术时预防性脾切除对有脾门淋巴结转移者并不无益于长期生存，而对无脾门淋巴结转移病例，未作脾切除的反而存活率高。脾切除组还存在术后感染率高，复发死亡较快等现象。医科院肿瘤医院937例报告中，有10例行全胃切除术。其中9例在1年内死亡，1例没有活过2年。胃次全切除合并切除脾、胰尾者20例。术后死亡2例，有2例存活5年以上（1例6年，另1例8年）。作者同意一些人的观点，贲门癌由于就诊时多数已属晚期，早已存在淋巴结转移，根治手术是无助益的。假如肿瘤确实还是局限时，根治手术又无必要。对于局限于贲门部不超过小弯长度的1/3的病变，应行胃次全切除术加区域淋巴结清扫，是比较合适的治疗方针。
（三）贲门癌的外科治疗近远期疗效
贲门癌的手术疗效比食管癌要差。国内三大组切除率73.7%～82.1%，切除死亡率1.7%～2.4%。三大组的5年生存率19.0%～24.0%，10年生存率8.6%～14.3%。
影响贲门癌远期生存的主要因素为淋巴结有无转移，肿瘤是否浸润浆膜以及切除性质（根治或姑息）。贲门癌的国际TNM分期，由于综合了前两个可变因素，同样是预测病人转归的有效指标。
（四）残胃贲门癌
远侧胃部分切除术后残胃囊发生癌的报告日益增多。其发生率为0.55%～8.9%，其中发生在贲门部的占全部的16.4%～58.5%，残胃贲门癌在贲门癌中的发生率为1.5%～2.7%。
残胃癌的定义：
1.首次胃次全切除是治疗良性疾病，如胃或十二指肠溃疡。
2.距首次胃部分切除到发生癌瘤间隔期不少于5年。一般认为多发生于毕氏Ⅱ式术后，但也有持相反意见的。首次胃切除术后胃酸分泌减少，十二指肠液反流刺激，萎缩性胃炎及肠上皮化生的存在皆为可能的诱因。
迄今为止，手术治疗是公认的贲门癌的首选治疗。由于其组织学为腺癌或粘液腺癌，放射治疗几乎无效，化学治疗效果也甚微。贲门癌手术适应证：①经X线、细胞学及内镜确诊；②超声检查、腹部CT扫描或腹腔镜检除外淋巴结、肝、肾上腺、网膜、腹膜及盆腔转移，无腹水；③一般情况中等以上，无重大心肺或其他脏器合并症。
由于贲门的解剖学特点，与肝、脾、横结肠、胰尾、肾、肾上腺、小肠、膈肌、后腹膜等诸多脏器相邻，又具有丰富的淋巴引流，向上入纵隔，向下沿大弯及小弯两条主要通道扩散，还可在胃壁内浸润，甚至达到全胃，因此一般的消化道造影不可能显示全部上述各个进程，应用发泡剂双重对比造影，可以清楚显示肿块、软组织影、粘膜破坏、溃疡、胃壁增厚的范围等，但X线改变常要比实际情况轻。应用腹部CT，可以了解肿物与周围器官之关系，但是比较食管的CT所见，贲门癌的阳性发现往往不太肯定，譬如是否侵及胰，往往判断不正确，CT怀疑有胰尾浸润而实际并无粘连，CT认为与胰无关联，但开腹肿瘤与胰浸润粘连成团。CT有助于发现肝转移，但对局部淋巴结转移的判断就不太准确。总之，在术前判断贲门癌之发展程度，估计其切除可能性等是一件相当困难的事，是临床到目前尚未解决的难题。为了不使病人失去治疗机会。腹部B超、CT以及食管胃造影等检查的阳性发现，除非确证已有广泛扩散转移，都应给予探查，争取切除病变并恢复消化道连续性。
（二）贲门癌的手术途径及方法
医科院肿瘤医院胸外科习惯采用左胸后外侧标准开胸切口，经第7肋床或肋间，然后在左膈顶部以食管为轴心作辐射状切口开腹。此种径路，对贲门区显露良好，足以行次全胃切除及胃周及胃左血管的淋巴结清扫。如需要扩大切除范围，行全胃或合并切除脾、部分胰等，则可将该切口向前下延到上腹壁，切断左肋软骨弓膈肌及腹壁肌肉，很方便地变成胸腹联合切口，充分显露上腹部。
在心肺功能储备低下和高龄病人中，可以采用颈腹二切口非开胸食管内翻拨脱部分胃切除，食管胃颈部吻合术。先开腹探查病变可以切除后，通过胃底或腹段食管开口将食管探条送到颈部，此时颈部食管已经显露，在准备作吻合部位之下方将食管结扎固定在探条上，切断上方食管，持续而均匀地牵拉探条，将食管自上而下翻转拔脱。游离胃常规切除部分胃，大弯剪裁成管状，经食管床上提入颈与食管吻合，这种手术的缺点是胃切除范围受限，可以导致胃侧切缘不净有残余癌。当纵隔过去有炎症，如淋巴结核而发生粘连时，会使翻转拔脱遇到困难，拔不动或是撕裂气管支气管膜部，发生后一种情况时需立即开胸修补，如事先已经估计拔脱有困难时，最好采用开胸切除的办法。
对心肺功能不足病人还有一种手术径路，就是联合胸骨正中切开和上腹正中切口，术中注意防止双侧胸膜破裂，并将心包自膈面游离，中线切开膈肌达食管裂孔，将心包前提显露后纵膈，然后常规将贲门癌及下段食管切除，残胃上提在后纵隔与食管吻合。此种切口显露后纵隔受一定限制，可以使用食管胃机械吻合器以保证吻合口质量。
常用的手术方法是近侧胃次全切除术。适应于贲门部肿瘤体积不大，沿小弯侵延不超过其全长的1/3时。手术具体操作如下：左后外第7肋床或肋间开胸，探查下段食管，然后以裂孔为轴心向左前切开膈肌、探腹，无肝、腹膜转移或广泛淋巴结转移时，沿大弯离断大网膜、左胃网膜动脉和胃脾韧带中的胃短动脉，离断左侧膈肌脚，完全显露下段食管，清除该部位（包括下肺韧带内）淋巴结。纱布垫开胰体及尾，显露胃左血管及其附近的淋巴结，仔细清扫淋巴结，结扎切断胃左血管，离断肝胃韧带，近侧胃完全游离，在大弯侧裁制胃管，如有胃缝合机可节省操作时间。要求切缘距肿瘤边不＜5cm。将胃管顺时针旋转90°，然后与食管下残端对端吻合，里层是全层结节缝合，外层将胃浆肌层向上套叠包绕吻合口约2cm，如望远镜状。吻合前为防止胃口粘膜过长，外翻覆盖肌层边影响吻合操作，可先环状切开胃管口部肌层，此时松弛的粘膜由于远侧肌层回缩而如袖状裸露。充分作粘膜下层止血，齐远侧肌层平面剪除多余之粘膜，此时胃管口的粘膜正好与肌层相平，吻合时视野十分清晰，有助于严密对合。
肿瘤浸润超过胃小弯长度一半时需行全胃切除，需离断全部5组胃的血供，全胃切除后缝合十二指肠端，作食管空肠吻合术。最简单的是食管空肠端侧吻合，空肠空肠侧侧吻合术，或者是Roux-Y食管空肠对端吻合，空肠空肠端侧吻合术。作者认为前者操作较简，空肠血运较后者保存更好。
如肿瘤已侵及胃脾韧带或胰尾，则可在次全或全胃切除同时行脾、胰尾切除术。注意妥善缝合胰的切断面，最好再用大网膜覆盖，以防止发生胰管瘘。
贲门癌手术治疗时胃切除范围一直是有争议的问题。有主张一律行全胃切除，有的作者主张整块切除全胃、脾、胰尾、网膜及区域淋巴结取得改进的生存。也有比较次全及全胃切除术后疗效，发现两者之存活率并无差别，建议仅在肿瘤累及胃体时作全胃切除。还有的作者发现在全胃切除术时预防性脾切除对有脾门淋巴结转移者并不无益于长期生存，而对无脾门淋巴结转移病例，未作脾切除的反而存活率高。脾切除组还存在术后感染率高，复发死亡较快等现象。医科院肿瘤医院937例报告中，有10例行全胃切除术。其中9例在1年内死亡，1例没有活过2年。胃次全切除合并切除脾、胰尾者20例。术后死亡2例，有2例存活5年以上（1例6年，另1例8年）。作者同意一些人的观点，贲门癌由于就诊时多数已属晚期，早已存在淋巴结转移，根治手术是无助益的。假如肿瘤确实还是局限时，根治手术又无必要。对于局限于贲门部不超过小弯长度的1/3的病变，应行胃次全切除术加区域淋巴结清扫，是比较合适的治疗方针。
（三）贲门癌的外科治疗近远期疗效
贲门癌的手术疗效比食管癌要差。国内三大组切除率73.7%～82.1%，切除死亡率1.7%～2.4%。三大组的5年生存率19.0%～24.0%，10年生存率8.6%～14.3%。
影响贲门癌远期生存的主要因素为淋巴结有无转移，肿瘤是否浸润浆膜以及切除性质（根治或姑息）。贲门癌的国际TNM分期，由于综合了前两个可变因素，同样是预测病人转归的有效指标。
（四）残胃贲门癌
远侧胃部分切除术后残胃囊发生癌的报告日益增多。其发生率为0.55%～8.9%，其中发生在贲门部的占全部的16.4%～58.5%，残胃贲门癌在贲门癌中的发生率为1.5%～2.7%。
残胃癌的定义：
1.首次胃次全切除是治疗良性疾病，如胃或十二指肠溃疡。
2.距首次胃部分切除到发生癌瘤间隔期不少于5年。一般认为多发生于毕氏Ⅱ式术后，但也有持相反意见的。首次胃切除术后胃酸分泌减少，十二指肠液反流刺激，萎缩性胃炎及肠上皮化生的存在皆为可能的诱因。
贲门癌转移症状
1.直接浸润漫延
波及食管下端胃的其他部分，如裂孔部膈肌、肝左叶、肝胃韧带、胰尾、脾门、脾以及其他腹膜后结构。
2.淋巴道转移
如转移到贲门壁内，尤其是粘膜下和浆膜下层有丰富的淋巴网与食管淋巴网交通，汇集而成壁外淋巴管，向上引流纵隔，向下引流腹腔丛，最后进入胸导管。有作者提出贲门的3条淋巴引流系统：①升干，沿食管壁上行至纵隔；②右干，从胃小弯沿胃左血管和贲门食管支到腹腔动脉旁；③左干，向后壁沿大弯到胰上缘和腹膜后。又可分大弯支、后胃支及膈支。各系统沿线皆有淋巴结。属第一站的是贲门旁（左、右）、下段食管旁及胃小弯淋巴结，第二站有胃左血管旁、脾血管旁及网膜淋巴结。远处者有腹腔动脉旁、腹主动脉旁、肝门区、纵隔及锁上淋巴结。
3.血运转移
①经过门静脉入肝，通过下腔静脉入体循环；②经器官间静脉径路直接入体循环。前者是最常见转移通路。
4.种植
癌细胞可脱落种植到腹膜、网膜、盆腔等处，可伴发血性腹水。
波及食管下端胃的其他部分，如裂孔部膈肌、肝左叶、肝胃韧带、胰尾、脾门、脾以及其他腹膜后结构。
2.淋巴道转移
如转移到贲门壁内，尤其是粘膜下和浆膜下层有丰富的淋巴网与食管淋巴网交通，汇集而成壁外淋巴管，向上引流纵隔，向下引流腹腔丛，最后进入胸导管。有作者提出贲门的3条淋巴引流系统：①升干，沿食管壁上行至纵隔；②右干，从胃小弯沿胃左血管和贲门食管支到腹腔动脉旁；③左干，向后壁沿大弯到胰上缘和腹膜后。又可分大弯支、后胃支及膈支。各系统沿线皆有淋巴结。属第一站的是贲门旁（左、右）、下段食管旁及胃小弯淋巴结，第二站有胃左血管旁、脾血管旁及网膜淋巴结。远处者有腹腔动脉旁、腹主动脉旁、肝门区、纵隔及锁上淋巴结。
3.血运转移
①经过门静脉入肝，通过下腔静脉入体循环；②经器官间静脉径路直接入体循环。前者是最常见转移通路。
4.种植
癌细胞可脱落种植到腹膜、网膜、盆腔等处，可伴发血性腹水。
食管癌及贲门癌早期及晚期表现
早期及晚期表现
（一）早期表现：①咽下食物梗噎感，常因进食固体食物引起，第一次出现梗噎感后，不经治疗而自行消失，隔数日或数月再次出现。②胸骨后疼痛，常在咽下食物后发生，进食粗糙热食或刺激性食物时加重。③食物通过缓慢并有滞留感。④剑突下烧灼样刺痛，轻重不等，多在咽下食物时出现，食后减轻或消失。⑤咽部干燥与紧缩感，食物吞下不畅，并有轻微疼痛。⑥胸骨后闷胀不适。
（二）中、晚期症状
1.吞咽困难：进行性吞咽困难是食管癌的主要症状。初起时进食固体食物有梗噎感，以后逐渐呈进行性加重，甚至流质饮食亦不能咽下。吞咽困难的严重程度除与病期有关外，与肿瘤的类型亦有关系。缩窄型出现梗阻症状早而严重，溃疡型及腔内型出现梗阻症状较晚。
2.疼痛和呕吐：见于严重吞咽困难病例，多将刚进食之食物伴同唾液呕出呈粘液状。疼痛亦为常见症状，多位于胸骨后，肩胛间区，早期多呈间歇性，出现持续而严重的胸痛或背痛、需用止痛剂止痛者，为晚期肿瘤外侵的征象。
3.贲门癌患者可出现便血、贫血。
4.体重下降及恶病质：因长期吞咽困难，引起营养障碍，体重明显下降，消瘦明显。出现恶液质是肿瘤晚期的表现。
5.邻近器官受累的症状：肿瘤侵及邻近器官可引起相应的症状。
（三）体征
早期患者无明显体征。晚期病例可有锁骨上淋巴结肿大，消瘦及恶液质，晚期贲门癌患者多有上腹部压痛或包块。
（一）早期表现：①咽下食物梗噎感，常因进食固体食物引起，第一次出现梗噎感后，不经治疗而自行消失，隔数日或数月再次出现。②胸骨后疼痛，常在咽下食物后发生，进食粗糙热食或刺激性食物时加重。③食物通过缓慢并有滞留感。④剑突下烧灼样刺痛，轻重不等，多在咽下食物时出现，食后减轻或消失。⑤咽部干燥与紧缩感，食物吞下不畅，并有轻微疼痛。⑥胸骨后闷胀不适。
（二）中、晚期症状
1.吞咽困难：进行性吞咽困难是食管癌的主要症状。初起时进食固体食物有梗噎感，以后逐渐呈进行性加重，甚至流质饮食亦不能咽下。吞咽困难的严重程度除与病期有关外，与肿瘤的类型亦有关系。缩窄型出现梗阻症状早而严重，溃疡型及腔内型出现梗阻症状较晚。
2.疼痛和呕吐：见于严重吞咽困难病例，多将刚进食之食物伴同唾液呕出呈粘液状。疼痛亦为常见症状，多位于胸骨后，肩胛间区，早期多呈间歇性，出现持续而严重的胸痛或背痛、需用止痛剂止痛者，为晚期肿瘤外侵的征象。
3.贲门癌患者可出现便血、贫血。
4.体重下降及恶病质：因长期吞咽困难，引起营养障碍，体重明显下降，消瘦明显。出现恶液质是肿瘤晚期的表现。
5.邻近器官受累的症状：肿瘤侵及邻近器官可引起相应的症状。
（三）体征
早期患者无明显体征。晚期病例可有锁骨上淋巴结肿大，消瘦及恶液质，晚期贲门癌患者多有上腹部压痛或包块。
贲门癌病理改变
病理改变
（一）大体分型
1.进展期 胃肠道分型一般沿用Borrman分型，其基本分类的蕈状、溃疡Ⅰ型、溃疡Ⅱ型与浸润型。我国作者据此对贲门癌分为4型。①隆起型：肿瘤为边缘较清晰的向腔内隆起的肿块，呈菜花、结节巨块或息肉状，可有浅溃疡；②局限溃疡型：肿瘤为深溃疡，边缘组织如围堤状隆起，切面与正常组织境界清晰；③浸润溃疡型：溃疡之边缘不清晰，切面与周围组织分界不清；④浸润型：肿瘤在贲门壁内浸润生长，受累处均匀增厚，与周围组织无界限，周围粘膜常呈放射状收缩。
大体分型与组织学类型有关，①、②两型以高分化腺癌和粘液腺癌较多。浸润溃疡型中低分化腺癌及粘液腺癌的比例增多。浸润型则多数是低分化弥漫型的腺癌或粘液腺癌。外科治疗预后以隆起型最好，局限溃疡型第二，浸润溃疡型较差，浸润型最差。
贲门腺癌的组织学类型主要有二类：腺癌与有明显粘液分泌的粘液腺癌。此二类又根据分化程度各自分为高分化、低分化和弥漫型三个亚型。分化程度之高低与手术预后关系密切。除了腺癌与粘液腺癌、贲门癌还有一些少见的组织学类型，如腺鳞癌、未分化癌、类癌（嗜银细胞癌）以及癌肉瘤等。
2.早期 早期贲门癌大体形态与胃其他部位和食管的早期癌相似。可以简单分为三型，①凹陷型：癌瘤部粘膜呈不规则的轻度凹陷，有少数为浅溃疡，与周围正常粘膜分界不明确，镜下分化常较差；②隆起型：癌变部粘膜增厚粗糙，稍有隆起，部分表现为斑块、结节或息肉状，以高分化腺癌占多数；③隐伏型：病变部粘膜颜色略深，质地略粗，此外大体无明显改变，经组织学检查始确诊，是3型中比较最早的形态。
（二）贲门癌的组织发生
过去胃癌的组织发生学中，胃溃疡、胃息肉（腺瘤）及慢性萎缩性胃炎皆被认为是胃癌的癌前期病变。近年的研究发现上述几种情况发生癌变的机会很小。特别是在贲门部这三种情况比胃的其他部分更少发生。所以显然与贲门癌的组织发生关系不大。
目前比较被承认的观点是贲门癌起源于贲门腺的颈部干细胞，因有多方向分化的潜能，可以形成具有贲门或腺上皮特点的腺癌。多数贲门癌的光镜、电镜和组化研究发现是混合型，是该观点的有力支持，不典型增生是贲门癌的癌前病变，它也是在上述与贲门癌发病有关的溃疡、息肉、萎缩性胃炎共有的关键病理过程。当他们发生不典型增生的改变时才可能癌变，其中结肠型化生多数具有不典型增生的性质。
贲门癌的临床病理发期
1987年国际抗癌联盟UICC修改后的胃癌TNM分期法，其规定如下：
胃癌TNM分期
0期 Tis N0 M0
ⅠA期 T1 N0 M0
ⅠB期 T1 N1 M0
T2 N0 M0
Ⅱ期 T1 N2 M0
T2 N1 M0
T3 N0 M0
ⅢA期 T2 N2 M0
T3 N1 M0
T4 N0 M0
ⅢB期 T3 N2 M0
T4 N2 M0
Ⅳ期 T4 N2 M0
任T 任N M1
T指原发肿瘤：Tis原位癌在表皮内尚未侵及固有层，T1肿瘤侵及固有层或粘膜下，T2肿瘤侵及肌层及浆膜下，T3肿瘤穿透浆膜（脏层腹膜），未达相邻结构，T4肿瘤侵及相邻结构（指脾、横结肠、肝、膈肌、胰、腹壁、肾上腺、肾、小肠及后腹膜）。
N指区域淋巴结，N0无区域淋巴结转移，N1胃周距肿瘤周边3cm以内淋巴结转移，N2胃周距肿瘤周边3cm以外淋巴结转移，或沿胃左、肝总、脾及腹腔动脉的淋巴结转移。
M指远处转移，M0无远处转移，M1有远处转移。还可标明转移部位，如：肺为PUL，骨为OSS，肝为HEP，脑为BRA，腹膜为PER等。
医科院肿瘤医院报告的937例贲门癌中TNM分期有资料可查的629例，其中Ⅰ期152例（24.1%），Ⅱ期179例（28.5%），Ⅲ期298例（47.4%）。由此可见到医院来就医的贲门癌中3/4（75.9%）属Ⅱ、Ⅲ期，仅约1/4的病例病期尚早。
（一）大体分型
1.进展期 胃肠道分型一般沿用Borrman分型，其基本分类的蕈状、溃疡Ⅰ型、溃疡Ⅱ型与浸润型。我国作者据此对贲门癌分为4型。①隆起型：肿瘤为边缘较清晰的向腔内隆起的肿块，呈菜花、结节巨块或息肉状，可有浅溃疡；②局限溃疡型：肿瘤为深溃疡，边缘组织如围堤状隆起，切面与正常组织境界清晰；③浸润溃疡型：溃疡之边缘不清晰，切面与周围组织分界不清；④浸润型：肿瘤在贲门壁内浸润生长，受累处均匀增厚，与周围组织无界限，周围粘膜常呈放射状收缩。
大体分型与组织学类型有关，①、②两型以高分化腺癌和粘液腺癌较多。浸润溃疡型中低分化腺癌及粘液腺癌的比例增多。浸润型则多数是低分化弥漫型的腺癌或粘液腺癌。外科治疗预后以隆起型最好，局限溃疡型第二，浸润溃疡型较差，浸润型最差。
贲门腺癌的组织学类型主要有二类：腺癌与有明显粘液分泌的粘液腺癌。此二类又根据分化程度各自分为高分化、低分化和弥漫型三个亚型。分化程度之高低与手术预后关系密切。除了腺癌与粘液腺癌、贲门癌还有一些少见的组织学类型，如腺鳞癌、未分化癌、类癌（嗜银细胞癌）以及癌肉瘤等。
2.早期 早期贲门癌大体形态与胃其他部位和食管的早期癌相似。可以简单分为三型，①凹陷型：癌瘤部粘膜呈不规则的轻度凹陷，有少数为浅溃疡，与周围正常粘膜分界不明确，镜下分化常较差；②隆起型：癌变部粘膜增厚粗糙，稍有隆起，部分表现为斑块、结节或息肉状，以高分化腺癌占多数；③隐伏型：病变部粘膜颜色略深，质地略粗，此外大体无明显改变，经组织学检查始确诊，是3型中比较最早的形态。
（二）贲门癌的组织发生
过去胃癌的组织发生学中，胃溃疡、胃息肉（腺瘤）及慢性萎缩性胃炎皆被认为是胃癌的癌前期病变。近年的研究发现上述几种情况发生癌变的机会很小。特别是在贲门部这三种情况比胃的其他部分更少发生。所以显然与贲门癌的组织发生关系不大。
目前比较被承认的观点是贲门癌起源于贲门腺的颈部干细胞，因有多方向分化的潜能，可以形成具有贲门或腺上皮特点的腺癌。多数贲门癌的光镜、电镜和组化研究发现是混合型，是该观点的有力支持，不典型增生是贲门癌的癌前病变，它也是在上述与贲门癌发病有关的溃疡、息肉、萎缩性胃炎共有的关键病理过程。当他们发生不典型增生的改变时才可能癌变，其中结肠型化生多数具有不典型增生的性质。
贲门癌的临床病理发期
1987年国际抗癌联盟UICC修改后的胃癌TNM分期法，其规定如下：
胃癌TNM分期
0期 Tis N0 M0
ⅠA期 T1 N0 M0
ⅠB期 T1 N1 M0
T2 N0 M0
Ⅱ期 T1 N2 M0
T2 N1 M0
T3 N0 M0
ⅢA期 T2 N2 M0
T3 N1 M0
T4 N0 M0
ⅢB期 T3 N2 M0
T4 N2 M0
Ⅳ期 T4 N2 M0
任T 任N M1
T指原发肿瘤：Tis原位癌在表皮内尚未侵及固有层，T1肿瘤侵及固有层或粘膜下，T2肿瘤侵及肌层及浆膜下，T3肿瘤穿透浆膜（脏层腹膜），未达相邻结构，T4肿瘤侵及相邻结构（指脾、横结肠、肝、膈肌、胰、腹壁、肾上腺、肾、小肠及后腹膜）。
N指区域淋巴结，N0无区域淋巴结转移，N1胃周距肿瘤周边3cm以内淋巴结转移，N2胃周距肿瘤周边3cm以外淋巴结转移，或沿胃左、肝总、脾及腹腔动脉的淋巴结转移。
M指远处转移，M0无远处转移，M1有远处转移。还可标明转移部位，如：肺为PUL，骨为OSS，肝为HEP，脑为BRA，腹膜为PER等。
医科院肿瘤医院报告的937例贲门癌中TNM分期有资料可查的629例，其中Ⅰ期152例（24.1%），Ⅱ期179例（28.5%），Ⅲ期298例（47.4%）。由此可见到医院来就医的贲门癌中3/4（75.9%）属Ⅱ、Ⅲ期，仅约1/4的病例病期尚早。
我奶奶得了 喷门癌 贲门癌
我奶奶得了 喷门癌 贲门癌
贴出来喷门癌 贲门癌的简介给大家分享
贲门癌在我国食管癌高发区的发病率也很高，据这些地区及肿瘤研治机构的统计，食管癌与贲门癌的比例约为2∶1。正确的贲门癌定义是发生在胃贲门部，也就是食管胃交界线下约2cm范围内的腺癌。它是胃癌的特殊类型，应和食管下段癌区分。但是它又与其他部位的胃癌不同，具有自己的解剖学组织学特性和临床表现，独特的诊断和治疗方法以及较差的外科治疗效果。
（一）大体分型
1.进展期 胃肠道分型一般沿用Borrman分型，其基本分类的蕈状、溃疡Ⅰ型、溃疡Ⅱ型与浸润型。我国作者据此对贲门癌分为4型。①隆起型：肿瘤为边缘较清晰的向腔内隆起的肿块，呈菜花、结节巨块或息肉状，可有浅溃疡；②局限溃疡型：肿瘤为深溃疡，边缘组织如围堤状隆起，切面与正常组织境界清晰；③浸润溃疡型：溃疡之边缘不清晰，切面与周围组织分界不清；④浸润型：肿瘤在贲门壁内浸润生长，受累处均匀增厚，与周围组织无界限，周围粘膜常呈放射状收缩。
大体分型与组织学类型有关，①、②两型以高分化腺癌和粘液腺癌较多。浸润溃疡型中低分化腺癌及粘液腺癌的比例增多。浸润型则多数是低分化弥漫型的腺癌或粘液腺癌。外科治疗预后以隆起型最好，局限溃疡型第二，浸润溃疡型较差，浸润型最差。
贲门腺癌的组织学类型主要有二类：腺癌与有明显粘液分泌的粘液腺癌。此二类又根据分化程度各自分为高分化、低分化和弥漫型三个亚型。分化程度之高低与手术预后关系密切。除了腺癌与粘液腺癌、贲门癌还有一些少见的组织学类型，如腺鳞癌、未分化癌、类癌（嗜银细胞癌）以及癌肉瘤等。
2.早期 早期贲门癌大体形态与胃其他部位和食管的早期癌相似。可以简单分为三型，①凹陷型：癌瘤部粘膜呈不规则的轻度凹陷，有少数为浅溃疡，与周围正常粘膜分界不明确，镜下分化常较差；②隆起型：癌变部粘膜增厚粗糙，稍有隆起，部分表现为斑块、结节或息肉状，以高分化腺癌占多数；③隐伏型：病变部粘膜颜色略深，质地略粗，此外大体无明显改变，经组织学检查始确诊，是3型中比较最早的形态。
（二）贲门癌的组织发生
过去胃癌的组织发生学中，胃溃疡、胃息肉（腺瘤）及慢性萎缩性胃炎皆被认为是胃癌的癌前期病变。近年的研究发现上述几种情况发生癌变的机会很小。特别是在贲门部这三种情况比胃的其他部分更少发生。所以显然与贲门癌的组织发生关系不大。
目前比较被承认的观点是贲门癌起源于贲门腺的颈部干细胞，因有多方向分化的潜能，可以形成具有贲门或腺上皮特点的腺癌。多数贲门癌的光镜、电镜和组化研究发现是混合型，是该观点的有力支持，不典型增生是贲门癌的癌前病变，它也是在上述与贲门癌发病有关的溃疡、息肉、萎缩性胃炎共有的关键病理过程。当他们发生不典型增生的改变时才可能癌变，其中结肠型化生多数具有不典型增生的性质。
贴出来喷门癌 贲门癌的简介给大家分享
贲门癌在我国食管癌高发区的发病率也很高，据这些地区及肿瘤研治机构的统计，食管癌与贲门癌的比例约为2∶1。正确的贲门癌定义是发生在胃贲门部，也就是食管胃交界线下约2cm范围内的腺癌。它是胃癌的特殊类型，应和食管下段癌区分。但是它又与其他部位的胃癌不同，具有自己的解剖学组织学特性和临床表现，独特的诊断和治疗方法以及较差的外科治疗效果。
（一）大体分型
1.进展期 胃肠道分型一般沿用Borrman分型，其基本分类的蕈状、溃疡Ⅰ型、溃疡Ⅱ型与浸润型。我国作者据此对贲门癌分为4型。①隆起型：肿瘤为边缘较清晰的向腔内隆起的肿块，呈菜花、结节巨块或息肉状，可有浅溃疡；②局限溃疡型：肿瘤为深溃疡，边缘组织如围堤状隆起，切面与正常组织境界清晰；③浸润溃疡型：溃疡之边缘不清晰，切面与周围组织分界不清；④浸润型：肿瘤在贲门壁内浸润生长，受累处均匀增厚，与周围组织无界限，周围粘膜常呈放射状收缩。
大体分型与组织学类型有关，①、②两型以高分化腺癌和粘液腺癌较多。浸润溃疡型中低分化腺癌及粘液腺癌的比例增多。浸润型则多数是低分化弥漫型的腺癌或粘液腺癌。外科治疗预后以隆起型最好，局限溃疡型第二，浸润溃疡型较差，浸润型最差。
贲门腺癌的组织学类型主要有二类：腺癌与有明显粘液分泌的粘液腺癌。此二类又根据分化程度各自分为高分化、低分化和弥漫型三个亚型。分化程度之高低与手术预后关系密切。除了腺癌与粘液腺癌、贲门癌还有一些少见的组织学类型，如腺鳞癌、未分化癌、类癌（嗜银细胞癌）以及癌肉瘤等。
2.早期 早期贲门癌大体形态与胃其他部位和食管的早期癌相似。可以简单分为三型，①凹陷型：癌瘤部粘膜呈不规则的轻度凹陷，有少数为浅溃疡，与周围正常粘膜分界不明确，镜下分化常较差；②隆起型：癌变部粘膜增厚粗糙，稍有隆起，部分表现为斑块、结节或息肉状，以高分化腺癌占多数；③隐伏型：病变部粘膜颜色略深，质地略粗，此外大体无明显改变，经组织学检查始确诊，是3型中比较最早的形态。
（二）贲门癌的组织发生
过去胃癌的组织发生学中，胃溃疡、胃息肉（腺瘤）及慢性萎缩性胃炎皆被认为是胃癌的癌前期病变。近年的研究发现上述几种情况发生癌变的机会很小。特别是在贲门部这三种情况比胃的其他部分更少发生。所以显然与贲门癌的组织发生关系不大。
目前比较被承认的观点是贲门癌起源于贲门腺的颈部干细胞，因有多方向分化的潜能，可以形成具有贲门或腺上皮特点的腺癌。多数贲门癌的光镜、电镜和组化研究发现是混合型，是该观点的有力支持，不典型增生是贲门癌的癌前病变，它也是在上述与贲门癌发病有关的溃疡、息肉、萎缩性胃炎共有的关键病理过程。当他们发生不典型增生的改变时才可能癌变，其中结肠型化生多数具有不典型增生的性质。
2009年1月12日星期一
纵隔肿瘤
纵隔位于两侧肺之间，以胸骨和胸椎为其前后界。内有许多重要器官，有大血管、气管、主支气管、心包、食管、胸腺及大量脂肪、神经和淋巴管等组织，因先天发育过程异常或后天性囊肿或肿瘤形成，就成为纵隔肿瘤。纵隔内肿瘤种类繁多，有原发的、有转移的，原发肿瘤中以良性多见，但也有相当一部分为恶性。为标明病变在纵隔所在部位，可将纵隔划分为若干部分，以胸骨与第4胸椎下缘水平分为上、下两部，将含有很多重要器官的纵隔间隙称为“内脏器官纵隔”（中纵隔），右气管、心包前的间隙为前纵隔；在气管、心包后方（包括食管和脊柱旁纵隔）称为后纵隔。 据国内统计资料显示，纵隔肿瘤发病率以神经源性肿瘤占第一位，其次为畸胎类、胸腺肿瘤和甲状原肿瘤，各种囊性肿瘤最少。
肿瘤化疗
化疗指的是运用药物治疗疾病的方法。手术和放疗杀伤特定部位的癌细胞，而化疗对人体全身起作用。化疗可以消灭已扩散到全身各部位的癌细胞。目前，大约有90多种化疗药物被用于癌症治疗。这些化疗药物在化学成分、使用方法、治疗某种癌症的疗效和副作用上都各不相同。
化学治疗的目的主要分为三层。第一层是治愈癌症，意思就是使肿瘤或恶瘤消失，不会重新长出来。如果达不到这个目标，第二层目的就是控制疾病（抑制癌瘤生长和扩散），为癌症病人提供最好的生活质量。有时癌症到中晚期后，治愈和控制已不可能，治疗的目的只能是缓解。缓解的意思就是指使用化疗药物减轻癌症引起的症状，提高病人的生活质量（即使这不能延长他们的生命）。
虽然单用一种药物也可治疗癌症，但通常为了增强疗效，都是联合使用几种药物。合用具有不同作用的几种药物，可以杀死更多的癌细胞，以及降低人体对某种特定药物产生耐药性的可能。
化疗方式
化疗药物的摄入有很多种方式。它们可以口服；外敷；静脉注射；肌肉注射；皮下注射；动脉注射（进入动脉）；鞘内注射（通过脑脊髓流动进入中枢神经系统）；胸膜注射（进入胸腔）；腹膜注射（进入腹腔）；膀胱注射（进入膀胱）；阻断注射（进入肿瘤）。
化疗药物的选择
医生会决定最适合病人的药物种类、剂量和操作方式，以及治疗周期。医生的这些决定取决于癌症的类型、部位、癌变程度、对人体正常功能的影响程度以及病人的健康情况。
化疗方案可以单用一种药物，也可以合用几种药物。对大多数癌症病人，医生都会合用几种药物。几种药物合用，可以几种方式攻击癌细胞，从而比单用一种药物更有疗效。不同的药物可能导致不同的副作用，使用几种适度剂量的药物导致的副作用还可以忍受；不象只使用一种剂量很高的药物，导致的副作用非常严重，甚至对某种重要器官造成永久损害。医生给病人的药物量既要能治疗癌症，又要使副作用降到最小。医生会避免使用具有类似副作用的药物。
为了更好地合用几种化疗药物，医生必须考虑化疗药物之间以及化疗药物与别的药物（包括维生素和非处方药）之间可能存在的相互作用。某些情况下，这些相互作用会加重副作用，或妨碍化疗的效果。因此，病人在服用维生素和非处方药时，应告诉医生。
医生对癌症患者的建议是：
1）化疗时，如果医生没有为了某种原因给你开维生素，你就最好不要自行服用。
2）化疗结束后，询问医生何时可以服用维生素。
3）病人食用平衡饮食，可获得足够的维生素。
化疗药物的种类
化疗药物依据它们的作用机制分为几大类：
1）烷化剂：
烷化剂直接作用于DNA上，防止癌细胞再生。此类药物对慢性白血病、恶性淋巴瘤、何杰金氏病、多发性骨髓瘤、肺癌、乳腺癌和卵巢癌具有疗效。
烷化剂主要有白消安、顺氯氨铂、环磷酰胺（癌得星）、氮烯咪胺、异环磷酰胺、二氯甲二乙胺（盐酸氮芥）和苯丙氨酸氮芥。
2）抗代谢药：抗代谢药干扰DNA和RNA的合成，用于治疗慢性白血病、乳腺癌、卵巢癌、胃癌和结直肠癌。抗代谢药主要有5-氟脲嘧啶、甲氨蝶呤、阿糖胞苷和环胞苷。
3）抗肿瘤抗生素：抗肿瘤抗生素通过抑制酶的作用和有丝分裂或改变细胞膜来干扰DNA。抗肿瘤抗生素为细胞周期非特异性药物，广泛用于对癌症的治疗。抗肿瘤抗生素主要有博来霉素、更生霉素、红必霉素、阿霉素和黄胆素。
4）植物类抗癌药：植物类抗癌药都是植物碱和天然产品，它们可以抑制有丝分裂或酶的作用，从而防止细胞再生必需的蛋白质合成。植物类抗癌药常与其它抗癌药合用于多种癌瘤的治疗。植物类抗癌药主要有长春碱、长春新碱、三尖杉酯碱、足叶乙甙和威蒙。
5）杂类：另外一些化疗药物具有不同的作用机制，不属于上面几类。其中包括门冬酰胺酶和维甲酸。
6）激素：皮质类固醇激素用于治疗淋巴瘤、白血病和多发性骨髓瘤等癌症。当激素用于杀死癌细胞或减缓癌细胞生长时，可以把它们看成化疗药物。皮质类固醇激素有强的松和氟美松。性激素用于减缓乳腺癌、前列腺癌和子宫内膜癌的生长。它包括雌激素、抗雌激素、黄体酮和男性激素。性激素的作用方式不同于细胞毒素药物，属于特殊的化疗范畴。
7）免疫制剂：免疫制剂可以刺激癌症病人的免疫系统更有效地识别和攻击癌细胞。它们属于特殊的化疗范畴。（参见免疫治疗）
化学治疗的目的主要分为三层。第一层是治愈癌症，意思就是使肿瘤或恶瘤消失，不会重新长出来。如果达不到这个目标，第二层目的就是控制疾病（抑制癌瘤生长和扩散），为癌症病人提供最好的生活质量。有时癌症到中晚期后，治愈和控制已不可能，治疗的目的只能是缓解。缓解的意思就是指使用化疗药物减轻癌症引起的症状，提高病人的生活质量（即使这不能延长他们的生命）。
虽然单用一种药物也可治疗癌症，但通常为了增强疗效，都是联合使用几种药物。合用具有不同作用的几种药物，可以杀死更多的癌细胞，以及降低人体对某种特定药物产生耐药性的可能。
化疗方式
化疗药物的摄入有很多种方式。它们可以口服；外敷；静脉注射；肌肉注射；皮下注射；动脉注射（进入动脉）；鞘内注射（通过脑脊髓流动进入中枢神经系统）；胸膜注射（进入胸腔）；腹膜注射（进入腹腔）；膀胱注射（进入膀胱）；阻断注射（进入肿瘤）。
化疗药物的选择
医生会决定最适合病人的药物种类、剂量和操作方式，以及治疗周期。医生的这些决定取决于癌症的类型、部位、癌变程度、对人体正常功能的影响程度以及病人的健康情况。
化疗方案可以单用一种药物，也可以合用几种药物。对大多数癌症病人，医生都会合用几种药物。几种药物合用，可以几种方式攻击癌细胞，从而比单用一种药物更有疗效。不同的药物可能导致不同的副作用，使用几种适度剂量的药物导致的副作用还可以忍受；不象只使用一种剂量很高的药物，导致的副作用非常严重，甚至对某种重要器官造成永久损害。医生给病人的药物量既要能治疗癌症，又要使副作用降到最小。医生会避免使用具有类似副作用的药物。
为了更好地合用几种化疗药物，医生必须考虑化疗药物之间以及化疗药物与别的药物（包括维生素和非处方药）之间可能存在的相互作用。某些情况下，这些相互作用会加重副作用，或妨碍化疗的效果。因此，病人在服用维生素和非处方药时，应告诉医生。
医生对癌症患者的建议是：
1）化疗时，如果医生没有为了某种原因给你开维生素，你就最好不要自行服用。
2）化疗结束后，询问医生何时可以服用维生素。
3）病人食用平衡饮食，可获得足够的维生素。
化疗药物的种类
化疗药物依据它们的作用机制分为几大类：
1）烷化剂：
烷化剂直接作用于DNA上，防止癌细胞再生。此类药物对慢性白血病、恶性淋巴瘤、何杰金氏病、多发性骨髓瘤、肺癌、乳腺癌和卵巢癌具有疗效。
烷化剂主要有白消安、顺氯氨铂、环磷酰胺（癌得星）、氮烯咪胺、异环磷酰胺、二氯甲二乙胺（盐酸氮芥）和苯丙氨酸氮芥。
2）抗代谢药：抗代谢药干扰DNA和RNA的合成，用于治疗慢性白血病、乳腺癌、卵巢癌、胃癌和结直肠癌。抗代谢药主要有5-氟脲嘧啶、甲氨蝶呤、阿糖胞苷和环胞苷。
3）抗肿瘤抗生素：抗肿瘤抗生素通过抑制酶的作用和有丝分裂或改变细胞膜来干扰DNA。抗肿瘤抗生素为细胞周期非特异性药物，广泛用于对癌症的治疗。抗肿瘤抗生素主要有博来霉素、更生霉素、红必霉素、阿霉素和黄胆素。
4）植物类抗癌药：植物类抗癌药都是植物碱和天然产品，它们可以抑制有丝分裂或酶的作用，从而防止细胞再生必需的蛋白质合成。植物类抗癌药常与其它抗癌药合用于多种癌瘤的治疗。植物类抗癌药主要有长春碱、长春新碱、三尖杉酯碱、足叶乙甙和威蒙。
5）杂类：另外一些化疗药物具有不同的作用机制，不属于上面几类。其中包括门冬酰胺酶和维甲酸。
6）激素：皮质类固醇激素用于治疗淋巴瘤、白血病和多发性骨髓瘤等癌症。当激素用于杀死癌细胞或减缓癌细胞生长时，可以把它们看成化疗药物。皮质类固醇激素有强的松和氟美松。性激素用于减缓乳腺癌、前列腺癌和子宫内膜癌的生长。它包括雌激素、抗雌激素、黄体酮和男性激素。性激素的作用方式不同于细胞毒素药物，属于特殊的化疗范畴。
7）免疫制剂：免疫制剂可以刺激癌症病人的免疫系统更有效地识别和攻击癌细胞。它们属于特殊的化疗范畴。（参见免疫治疗）
疾病自测保健康
一个人尤其是中老年人在日常生活中，如果平时多注意健康状况的自我监护，可以及时发现疾病，有利于及时诊治，避免意外发生。
一、自测胸闷气喘如果在安静的状态下总感到胸闷、胸堵或心悸怔忡，胸中突然蹦一下或停一下，或在上楼(3~5层)以后心跳气喘半小时左右，有时还可能有停跳(即期外收缩)，应及时到医院检查心脏，看有无冠状动脉供血不足的现象。这组症状经常是心脏功能不佳的最早表现。
二、自测食欲改变因疲劳或感冒偶尔一两顿饭不想吃是可以理解的，如果超过一星期就应警惕了，胃部及消化系统其他器官(肝、肠)的肿瘤通常有这些症状。有一种进食发噎的现象更应注意，正常速度进食或吞咽引发噎，吃干食品、连续吞咽过急会偶尔发噎，但如果总是发噎，并且愈来愈重，这种情况可能是食道肿瘤的征兆，要及时去医院检查。
三、自测排便异常正常人都有一定的大便习惯，中老年人如果两个月内排便的习惯发生了变化，时而便秘，时而腹泻，时而两三天才排一次便，有时却有一天两三次或更多次地排便，这是肠道功能紊乱的最早征象，必须进行检查。因大肠及直肠肿瘤，在早期就常有这类症状。
四、自测无端出血不该见血的地方，如果突然出血，要引起警惕，例如痰、粪便、尿、鼻涕中，不论是血丝、血点、血块，都应警惕。中老年人痰中带血，大多是肺部肿瘤的最早症状。总之，除去鼻子由于天气过于干燥，可能因局部微小血管破裂而引起出血外，一般排泄物或分泌物带血都不是好现象，必须引起注意。
五、自测头晕头痛如果清晨醒来，头脑仍是昏昏沉沉，头晕头痛，有可能是高血压或脑动脉开始硬化的迹象。偶尔发生一两次，可能是因为夜间失眠或多梦、噩梦造成的，如果经常发生上述症状，那就必须抓紧检查观察，找出原因所在。
六、自测四肢发麻凡是长期高血压的患者，如平白无故四肢发麻，有时甚至手脚大片麻木，有时则犹如昆虫在四肢爬行的痒麻感，再加上头痛头晕，这些都是中风的前兆，必须立即采取必要的措施，以防止脑卒中(中风)的发生。
七、自测连续咳嗽咳嗽是由于呼吸系统中的气管或支气管受到刺激，身体产生的一种保护性反射。平时无任何呼吸系统疾病也没感冒的中老年人，如果忽然经常咳嗽，就必须去做胸部检查。因为这种咳嗽有时是肺癌的最早信号，尤其是干咳、咳不出多少痰者，这是深部的支气管受到刺激的结果。
八、自测日渐消瘦这里指的是没有明显原因而日渐消瘦，有时在一两个月内体重减轻六七公斤或十来公斤。这种进行性的消瘦，大都表明体内有消耗性的疾病。对中老年人来说，主要是肿瘤的可能性较大。
九、自测口腔白斑口腔白斑是一种口腔黏膜角化病变，末期可有恶化趋势，它是口腔内常见的癌前病变之一，多发生于中老年人。白斑常发生于口腔内颊部、舌背及硬腭等部位，发病后局部黏膜会出现大小不一、外形不规则的白色斑块，稍增厚，表面粗黏，质地较硬，周围黏膜无炎性反应。患有口腔白斑的病人一般无自觉症状，倘若出现疼痛、溃烂，往往是恶性变的前兆，可转变为癌。因此，应引起高度重视，切莫麻痹大意。
十、自测排尿异常对男性中老年人来说，如果忽然出现尿频、尿急，每次排尿总像是没有排尽的感觉，这种情况有可能是男性的前列腺肥大或前列腺肿瘤在压迫尿道，需及时检查。
一、自测胸闷气喘如果在安静的状态下总感到胸闷、胸堵或心悸怔忡，胸中突然蹦一下或停一下，或在上楼(3~5层)以后心跳气喘半小时左右，有时还可能有停跳(即期外收缩)，应及时到医院检查心脏，看有无冠状动脉供血不足的现象。这组症状经常是心脏功能不佳的最早表现。
二、自测食欲改变因疲劳或感冒偶尔一两顿饭不想吃是可以理解的，如果超过一星期就应警惕了，胃部及消化系统其他器官(肝、肠)的肿瘤通常有这些症状。有一种进食发噎的现象更应注意，正常速度进食或吞咽引发噎，吃干食品、连续吞咽过急会偶尔发噎，但如果总是发噎，并且愈来愈重，这种情况可能是食道肿瘤的征兆，要及时去医院检查。
三、自测排便异常正常人都有一定的大便习惯，中老年人如果两个月内排便的习惯发生了变化，时而便秘，时而腹泻，时而两三天才排一次便，有时却有一天两三次或更多次地排便，这是肠道功能紊乱的最早征象，必须进行检查。因大肠及直肠肿瘤，在早期就常有这类症状。
四、自测无端出血不该见血的地方，如果突然出血，要引起警惕，例如痰、粪便、尿、鼻涕中，不论是血丝、血点、血块，都应警惕。中老年人痰中带血，大多是肺部肿瘤的最早症状。总之，除去鼻子由于天气过于干燥，可能因局部微小血管破裂而引起出血外，一般排泄物或分泌物带血都不是好现象，必须引起注意。
五、自测头晕头痛如果清晨醒来，头脑仍是昏昏沉沉，头晕头痛，有可能是高血压或脑动脉开始硬化的迹象。偶尔发生一两次，可能是因为夜间失眠或多梦、噩梦造成的，如果经常发生上述症状，那就必须抓紧检查观察，找出原因所在。
六、自测四肢发麻凡是长期高血压的患者，如平白无故四肢发麻，有时甚至手脚大片麻木，有时则犹如昆虫在四肢爬行的痒麻感，再加上头痛头晕，这些都是中风的前兆，必须立即采取必要的措施，以防止脑卒中(中风)的发生。
七、自测连续咳嗽咳嗽是由于呼吸系统中的气管或支气管受到刺激，身体产生的一种保护性反射。平时无任何呼吸系统疾病也没感冒的中老年人，如果忽然经常咳嗽，就必须去做胸部检查。因为这种咳嗽有时是肺癌的最早信号，尤其是干咳、咳不出多少痰者，这是深部的支气管受到刺激的结果。
八、自测日渐消瘦这里指的是没有明显原因而日渐消瘦，有时在一两个月内体重减轻六七公斤或十来公斤。这种进行性的消瘦，大都表明体内有消耗性的疾病。对中老年人来说，主要是肿瘤的可能性较大。
九、自测口腔白斑口腔白斑是一种口腔黏膜角化病变，末期可有恶化趋势，它是口腔内常见的癌前病变之一，多发生于中老年人。白斑常发生于口腔内颊部、舌背及硬腭等部位，发病后局部黏膜会出现大小不一、外形不规则的白色斑块，稍增厚，表面粗黏，质地较硬，周围黏膜无炎性反应。患有口腔白斑的病人一般无自觉症状，倘若出现疼痛、溃烂，往往是恶性变的前兆，可转变为癌。因此，应引起高度重视，切莫麻痹大意。
十、自测排尿异常对男性中老年人来说，如果忽然出现尿频、尿急，每次排尿总像是没有排尽的感觉，这种情况有可能是男性的前列腺肥大或前列腺肿瘤在压迫尿道，需及时检查。
以色列科学家发现治疗癌症新方法
以色列科学家新近研究发现，将两种按照要求制造出来的抗体进行正确组合，从而形成一个网，更有利于破坏癌细胞的通讯网络，最终使肌体得到康复。
经过对癌症30多年的研究，一种被称为“HER”的受体已经被鉴别出来，它们像天线一样安坐在细胞壁外部，暗示着某一种癌症的类型。魏兹曼研究院亚登教授领导的研究小组在研究中已经发现，在一定条件下，HER2受体可以增强细胞接收到的发育信号。为此，研究人员发明了一种方法培育出一些特定的抗体，这些抗体不仅可以独立地约束这些特殊的癌症受体，而且可以关闭与之相连的信号网。
在试管试验以及在实验鼠试验中，研究人员将癌细胞暴露在两个不同的抗体面前，让抗体与HER2受体相连接。在相互作用中，研究人员发现，对于受体构架中明显不同的附着点，这两种不同的抗体却显示出了合作性而不是竞争性，从而导致在受体之间出现一个大大的、有弹性的分子脚手架。连锁系统抓住并牵引着受体相互接近，直到因过载发生内部坍塌。这些受体被细胞吞噬，因而停止发信号。与之相应，细胞停止发育，若此时同时使用化疗与免疫疗法，将导致细胞的死亡。
亚登认为，他们的研究开辟了抗体－受体治疗系统的协作优势。研究结果证明，如果利用不同的抗体进行正确的协作，受体的退化将被加速，即在抑制HER2发信号方面，协作的效果要比只使用一种抗体大三倍以上。
亚登说：“了解HER受体的退化是如何进行的，就能够提高治疗效果，同时还为我们提供了一种方法，来使病人克服固有的或外来的对癌症治疗的抗性。”
经过对癌症30多年的研究，一种被称为“HER”的受体已经被鉴别出来，它们像天线一样安坐在细胞壁外部，暗示着某一种癌症的类型。魏兹曼研究院亚登教授领导的研究小组在研究中已经发现，在一定条件下，HER2受体可以增强细胞接收到的发育信号。为此，研究人员发明了一种方法培育出一些特定的抗体，这些抗体不仅可以独立地约束这些特殊的癌症受体，而且可以关闭与之相连的信号网。
在试管试验以及在实验鼠试验中，研究人员将癌细胞暴露在两个不同的抗体面前，让抗体与HER2受体相连接。在相互作用中，研究人员发现，对于受体构架中明显不同的附着点，这两种不同的抗体却显示出了合作性而不是竞争性，从而导致在受体之间出现一个大大的、有弹性的分子脚手架。连锁系统抓住并牵引着受体相互接近，直到因过载发生内部坍塌。这些受体被细胞吞噬，因而停止发信号。与之相应，细胞停止发育，若此时同时使用化疗与免疫疗法，将导致细胞的死亡。
亚登认为，他们的研究开辟了抗体－受体治疗系统的协作优势。研究结果证明，如果利用不同的抗体进行正确的协作，受体的退化将被加速，即在抑制HER2发信号方面，协作的效果要比只使用一种抗体大三倍以上。
亚登说：“了解HER受体的退化是如何进行的，就能够提高治疗效果，同时还为我们提供了一种方法，来使病人克服固有的或外来的对癌症治疗的抗性。”
测试自己得肺癌的危险有多大
肺癌是发生在人体肺脏的癌症。肺是人体呼吸系统的主要部份。人体的吐故纳新离不开肺。在美国，肺癌是所有癌症中的第一杀手。在中国，死于肺癌的人数也在增加。大多数肺癌在做出诊断的时候已经到了不治的晚期。吸烟与肺癌的发生密切相关，是引起大多数肺癌的首要原因。健康专家预测，如果美国所有吸烟的人都戒掉烟，全国没有人吸烟，美国的癌症会至少要减少三分之一。对自己得肺癌的危险心中有数，可以有的放矢地去消除肺癌的危险。下面这个关于肺癌的危险评价表可以告诉您得肺癌的具体危险。请在与自己情况相符的问题上打勾，最后将所得的分数相加，得出总分。然后，在结果解释表中了解自己得肺癌的危险是大还是小。
1、直系亲属(父母，兄弟姐妹，叔伯姑姨)中有没有人得肺癌？
有+1分无0
2、现在多少岁？
20-39岁1分
40-49岁2分
过了50岁3分
3、您过去是否曾经吸烟？
是4分
否0
4、现在吸烟吗？
吸烟4分
不吸烟0
5、果现在吸烟，每天吸多少？
每天少于一包1分
每天一包2分
每天一到一包半3分
每天至少二包4分
6、果已经戒烟，戒了多久？
不到5年- 1分
6-10年-2分
11-20年-3分
多于20年-4分
7、有没有和吸烟的人住在一起？
有3分
没有0
8、有没有在很多人吸烟的地方(酒吧，夜总会等)工作？
有3分
没有0
9、有没有被诊断患有慢性气管炎或肺气肿？
有2分
没有0
10、第4问题回答“是”
加5分
结果解释
少于7分危险很低
7-12分低到中度危险
13-18分中到高度危险
高于18分危险很高
1、直系亲属(父母，兄弟姐妹，叔伯姑姨)中有没有人得肺癌？
有+1分无0
2、现在多少岁？
20-39岁1分
40-49岁2分
过了50岁3分
3、您过去是否曾经吸烟？
是4分
否0
4、现在吸烟吗？
吸烟4分
不吸烟0
5、果现在吸烟，每天吸多少？
每天少于一包1分
每天一包2分
每天一到一包半3分
每天至少二包4分
6、果已经戒烟，戒了多久？
不到5年- 1分
6-10年-2分
11-20年-3分
多于20年-4分
7、有没有和吸烟的人住在一起？
有3分
没有0
8、有没有在很多人吸烟的地方(酒吧，夜总会等)工作？
有3分
没有0
9、有没有被诊断患有慢性气管炎或肺气肿？
有2分
没有0
10、第4问题回答“是”
加5分
结果解释
少于7分危险很低
7-12分低到中度危险
13-18分中到高度危险
高于18分危险很高
实验室和其他辅助检查方法
一、乳腺X线摄影
乳腺X线检查对多种乳房疾病具有较好的敏感性和特异性，特别是在鉴别良、恶性病变，早期诊断乳腺癌方面具有明显优势。乳腺X线检查对乳腺癌的诊断符合率可达90%以上，并能发现隐性乳腺癌，是目前公认的乳腺癌最有效、最可靠的诊断方法。临床上常用的乳腺X线摄影方法有乳腺钼靶X线摄影、乳腺导管造影和乳腺囊肿内充气造影。
（一）乳腺钼靶X线摄影
乳腺癌常见的钼靶X线表现包括直接征象和间接征象。
1．直接征象 乳腺癌癌灶本身所形成的影像称为乳腺癌的X线直接征象。
（1）肿块阴影：其为乳腺癌最常见和最基本的X线征象。临床乳腺癌中85%~90%的病例可见致密块影。①肿块形态，多呈分叶状、圆形、椭圆形或哑铃形；②肿块密度，中心区高于周边，或呈密度不均的征象；③肿块边缘，多有长短不一的毛刺或晕状影触角，呈发团影；④临床触诊的肿块大于X线的肿块，是恶性肿瘤的重要征象之一。
（2）恶性钙化：据统计，40%乳腺癌患者的X线片中有钙化出现。因此，钙化是乳腺癌的重要特征之一。X线所见恶性钙化常有三种形态。①小杆状钙化，多发生在导管内，常见于导管癌，若钙化填充在末支导管分叉处，则呈叉状钙化；②泥沙样钙化，多发生有肿块边缘，也可在导管内或腺泡中；③团簇状钙化，形态较前二者大且不规则，以发生在肿瘤坏死才有诊断价值。恶性钙化的特征为：钙化粒微小，密度高低不一，大小不等，呈不规则形态。单位面积内数目较多，从几个到数十个不等，有聚集性。成堆的细小钙化对乳腺癌诊断有意义，尤其在无明显肿块影时，当小杆状钙化和泥沙样钙化同时出现时，应高度怀疑乳腺癌。有人指出，每平方厘米在15个钙化点以上时，乳腺癌的可能性甚大；尤其在一丛钙化点中有2~3个小杆状钙化出现，即可诊断为乳腺癌。小叶内钙化常是小叶原位癌的唯一征象。
2．间接征象 乳腺癌癌灶周围继发性改变所形成的影像称为乳腺癌的X线间接征象。
（1）血管异常相：X线表现为：①患乳血管管轻（主要为静泳）较健侧增粗，一般左乳静脉比右乳粗，如果右乳静脉比左乳粗，且双乳血管比超过1：1：4时，应考虑乳腺癌的可能。②癌灶周围形成较多的细小血管丛，呈以癌灶为中心的放射状或排笔状。③癌灶区出现较粗大的引流静脉。
（2）透亮环影：肿块密度增高影的周围有一宽窄不一、密度低于肿块和外围的乳腺组织的环形透亮带。
（3）厚皮征：乳腺皮肤淋巴管被癌细胞浸润，导致皮肤充血、水肿、增厚，从而出现厚皮征。当癌肿反应性纤维化及收缩时，可出现皮肤扁平或“酒窝征”改变。
（4）乳头回缩：由于乳晕肿瘤粘连纤维化或癌肿侵及乳腺导管牵拉乳头所致。当乳头完全凹陷，单侧乳头在近期内回缩、固定者对临床诊断意义较大。
（5）大导管相：当癌瘤浸润大导管时，导管变粗而且有阴景增强表现，可以看到肿块与乳头之间出现粗大导管相，又称“癌桥”。或有时癌瘤向附近的导管浸润，造成多导管病变，与周围的血管、淋巴管及结缔组织融合，形成一条粗大的导管相。
（6）牛角征：Cooper氏韧带受癌瘤浸润后，在腺体与皮肤之间形成牛角形密影。其对乳腺癌诊断有重要价值，尤其连接肿块或致密结节影的牛角征更有特异性。
（7）塔尖征：癌瘤浸润淋巴管，致使淋巴管扩张及管内癌栓形成，从而可见一自肿块影向外笔直伸展的细条状致密影，状如塔尖。为乳腺癌的重要特征。
（8）乳房后间隙改变：深部乳腺癌可早期侵及浅筋膜的深层，导致乳房后间隙的透亮区消失。
（9）乳腺组织结构紊乱：不均匀低密度区及污秽的点片影。
（10）乳房形态改变：乳腺癌沿导管及腺体浸润时，尤其是向浅表浸润时，受累区膨出可致乳房变形。
（二）乳腺导管造影
乳腺导管造影不但可清晰显示乳腺导管及其细微结构，而且可以了解病变的部位及范围，弥补平片之不足，是早期发现微小癌的重要方法。对乳头溢液的良恶性乳腺疾病均有较大诊断价值。其主要用于不伴有乳房肿块的单个乳管呈血性、浆液性、水样乳头溢液者，或乳头溢液伴相应区域乳房包块诊断不明确者。
常见的乳腺导管造影恶性征象有：
1．导管本身因癌浸润、梗阻、破坏等引起的征象造影剂在大导管及二、三级分支表现为密度深浅不均，大小不一的“虫蚀征”；断续状分布的“断续征”；不规则充盈缺损；以及造景剂由导管破坏处向间质溢出形成大小不等之斑片状影的“潭湖征”。
2．因癌肿侵犯、收缩、压迫导管等引起的征象造影剂突然狭窄呈“鼠尾征”；一侧管壁僵直，突然中断等。亦可见虫蚀征。
（三）乳腺囊肿内充气造影
乳腺囊肿内充气造影主要用于临床与X线平片疑有乳腺囊性病变需确定性质，或疑有囊壁肿瘤需进一步确诊者。其恶生征象表现为：部分囊壁增厚，边缘不光整，甚至出现分叶状或毛刺状肿块等，则应首先考虑到癌变的可能。
二、超声检查
超声波检查对乳腺癌诊断准确率可达80%~85%，但对1cm以下者诊断准确率有待进一步提高。临床主要用于辅助X线检查之不足。
一般来说，恶性肿块边界不清，呈锯齿状，内部为低回声或强回声或不均匀回声，不同组织学类型的癌肿可使块后方回声增强或衰弱，肿块无滑动，无压缩，多数肿块长度大于深度。如皮肤局部回声线增厚、分层不清晰，乳头回缩，导管扩张，Cooper ′s韧带呈线性或三角形增厚，应高度重视有否早期乳癌。在恶性病变中，具有影像特征的如：①乳头状导管癌，乳头下方导管扩张呈分枝状，管内有强回声团突起。②硬癌，肿块不大，后方明显衰减。③髓样癌，呈球形，常为混合性回声，后方不衰减。
三、细胞学检查
细胞学检查包括：细钟吸取细胞学检查，乳头溢液涂片细胞学检查，乳头或肿瘤刮片细胞学检查及乳腺肿瘤切除标本印片细胞学检查。主要用于孤立病变，考虑为囊肿、良性或恶生肿瘤。临床明显的囊性病变、乳腺癌术后疤痕上孤立或多发的小结节、可疑的远处转移病灶、包括皮肤结节和肿大的淋巴结等可行诊断性穿刺。
四、活组织检查
用于乳腺诊断的活组织检查方法有切除活检、切取活检、穿刺活检、溃疡病灶的咬取活检、乳管内镜咬取活检等。
（一）切除活检
1．检查指征可触及的肿块，有痛性的肿块不能排除恶变者；非可及性肿块或X线上显示微小钙化；一个或两个乳管持续性自发性溢液；乳头的异常，乳头周围糜烂或近来自发性乳头回缩；乳腺皮肤的改变，如酒窝征、橘皮样变，或非炎症性皮肤改变；液窝淋巴结肿大；针吸细胞学检查阳性。
2．评价切除活检为临床常规方法，最为常用。既能达到活检的目的，又能达到治疗的目的，目前多主张此法。但冰冻检有时有假阳性或假阴性，应以否蜡活检为准。
（二）切取活检
1．检查指征基本同“切除活检”，适用于较大、已与皮肤粘连或已溃破的肿瘤。
2．评价切取活检有促进肿瘤转移的可能，除非肿瘤很大，尽量避免行切取活检。
（三）穿刺活检
1．检查指征乳房肿块考虑良性或恶性肿瘤；乳腺癌术后术区孤立或多发的小结节；可疑为转移的肿大淋巴结或皮肤结节，以及一切右通过穿刺取材部位的转移或可疑转移的病变。
2．评价易受穿刺针具和操作技术的影响，结果往往不十分可靠。操作时应避免造成肿瘤的播散。目前，利用高频X线电脑全自动定向活检装置，可对乳腺微小病变行准确定位，可望提高准确率。
（四）溃疡病灶咬取活检
适用于已破溃的肿瘤。一般在肿瘤破溃的边缘咬取部分进行肿瘤组织学检查及受体测定。取材时要避开坏死区，以免曩诊断，同时切忌挤压肿瘤组织。
（五）乳管内镜咬取活检
乳管内镜可确定病变的准确位置和性状，以及从乳管开口到病变部位的距离。此检查还可确认乳腺癌患侧乳管内的浸润情况，为施行保留乳头的乳腺癌根治术或保留乳房手术提供可靠依据。
五、热图检查
常用热图检查有液晶及远红外热图像两种方法。乳腺癌的热图像表现为：①局部放射热增加或出现热点；②局部血管增多或增粗、迂曲，可血管走向反常；③两侧温度明显不对称，患侧温度显著增高；④乳晕部热增加。但热图对较小肿瘤检出度低，假阳性及假阴性较多，经广泛评价后，目前大多已不将此法作为诊断乳腺癌而有明显异常温度记录者，可判断其预后较差。
六、近红外线乳腺扫描检查
乳腺癌的近红外线乳腺扫描图像表现为：限局性边缘不清的深灰或黑色的不均匀的吸光团，加压后不褪色（不发白），有时全乳呈深灰，需要增加探测器的亮度来得到与正常乳腺同机关报分辨率图像，周围有C型血管，双乳静脉系统的对称性消失，未受累乳腺呈正常表现，受累乳腺静脉扩张，呈广泛性扭曲和迂回，同时伴有静脉数量增加等。血管分型大多是VB4、VC2、VC3、VC4类型乳腺。液窝淋巴结呈现浅到深灰色卵圆形或圆形的均匀的灰色阴影。
乳腺癌近红外线图像有以下特点：①多级灰度倒环较多见，大部分为4级。②大多级倒环中3级灰度并不占据很大面积，点状和小片状3级灰度较多见。③在3级倒环周围，1~2级倒环面积较大，且分部不规则，尤其与中心的3级环无向心性分布。
近红外线检查对乳腺肿块诊断的准确率可达80%，且对乳腺充血性病变和血管的显示有一定特点，可作为一种辅助诊断方法。但对直径1cm以下的深部肿块易出现假阴性，宜与其他方法配合使用。
七、生物学标记检查
目前开展的生物学标记检查有癌胚抗原（CEA）、降钙素、含铁蛋白、单克隆抗体（CA15-3）等。生物学标记检查临床应用尚无足够的特异性和敏感性。应用多种标记物作为联合指标，可提高诊断价值，但亦只限于较晚期的乳腺癌病倒，对早期病倒亦无足够的敏感性。
八、PCR法癌基因诊断检查
K19和MUC1等检查与乳腺癌相关性较好，可检测出存在体内的微小转移灶。
九、激素受体检查
激素受体检查目前主要用于制订乳腺癌术后辅助治疗的方案及其预后的判断。目前用于临床的有：雌激素受体（ER）、孕激素受体（PR）检查。
十、其他检查
1．CT扫描CT扫描可用于不能扪及的乳腺病变组织检查前定位，确诊乳腺癌的手术前分期，检查乳腺后区、液部及内乳淋巴结有无肿大，有助于制订治疗计划。此法对纵隔、乳内淋巴结及胸骨病灶的诊断有极大的优势。但CT不是乳腺癌常规的诊断方法。
2．MRI MRI在鉴别良恶性病变，发现乳腺癌癌前病变可能有较大前景，但MRI不能显示微细钙化点，目前研究尚不能满足临床需要。
乳腺X线检查对多种乳房疾病具有较好的敏感性和特异性，特别是在鉴别良、恶性病变，早期诊断乳腺癌方面具有明显优势。乳腺X线检查对乳腺癌的诊断符合率可达90%以上，并能发现隐性乳腺癌，是目前公认的乳腺癌最有效、最可靠的诊断方法。临床上常用的乳腺X线摄影方法有乳腺钼靶X线摄影、乳腺导管造影和乳腺囊肿内充气造影。
（一）乳腺钼靶X线摄影
乳腺癌常见的钼靶X线表现包括直接征象和间接征象。
1．直接征象 乳腺癌癌灶本身所形成的影像称为乳腺癌的X线直接征象。
（1）肿块阴影：其为乳腺癌最常见和最基本的X线征象。临床乳腺癌中85%~90%的病例可见致密块影。①肿块形态，多呈分叶状、圆形、椭圆形或哑铃形；②肿块密度，中心区高于周边，或呈密度不均的征象；③肿块边缘，多有长短不一的毛刺或晕状影触角，呈发团影；④临床触诊的肿块大于X线的肿块，是恶性肿瘤的重要征象之一。
（2）恶性钙化：据统计，40%乳腺癌患者的X线片中有钙化出现。因此，钙化是乳腺癌的重要特征之一。X线所见恶性钙化常有三种形态。①小杆状钙化，多发生在导管内，常见于导管癌，若钙化填充在末支导管分叉处，则呈叉状钙化；②泥沙样钙化，多发生有肿块边缘，也可在导管内或腺泡中；③团簇状钙化，形态较前二者大且不规则，以发生在肿瘤坏死才有诊断价值。恶性钙化的特征为：钙化粒微小，密度高低不一，大小不等，呈不规则形态。单位面积内数目较多，从几个到数十个不等，有聚集性。成堆的细小钙化对乳腺癌诊断有意义，尤其在无明显肿块影时，当小杆状钙化和泥沙样钙化同时出现时，应高度怀疑乳腺癌。有人指出，每平方厘米在15个钙化点以上时，乳腺癌的可能性甚大；尤其在一丛钙化点中有2~3个小杆状钙化出现，即可诊断为乳腺癌。小叶内钙化常是小叶原位癌的唯一征象。
2．间接征象 乳腺癌癌灶周围继发性改变所形成的影像称为乳腺癌的X线间接征象。
（1）血管异常相：X线表现为：①患乳血管管轻（主要为静泳）较健侧增粗，一般左乳静脉比右乳粗，如果右乳静脉比左乳粗，且双乳血管比超过1：1：4时，应考虑乳腺癌的可能。②癌灶周围形成较多的细小血管丛，呈以癌灶为中心的放射状或排笔状。③癌灶区出现较粗大的引流静脉。
（2）透亮环影：肿块密度增高影的周围有一宽窄不一、密度低于肿块和外围的乳腺组织的环形透亮带。
（3）厚皮征：乳腺皮肤淋巴管被癌细胞浸润，导致皮肤充血、水肿、增厚，从而出现厚皮征。当癌肿反应性纤维化及收缩时，可出现皮肤扁平或“酒窝征”改变。
（4）乳头回缩：由于乳晕肿瘤粘连纤维化或癌肿侵及乳腺导管牵拉乳头所致。当乳头完全凹陷，单侧乳头在近期内回缩、固定者对临床诊断意义较大。
（5）大导管相：当癌瘤浸润大导管时，导管变粗而且有阴景增强表现，可以看到肿块与乳头之间出现粗大导管相，又称“癌桥”。或有时癌瘤向附近的导管浸润，造成多导管病变，与周围的血管、淋巴管及结缔组织融合，形成一条粗大的导管相。
（6）牛角征：Cooper氏韧带受癌瘤浸润后，在腺体与皮肤之间形成牛角形密影。其对乳腺癌诊断有重要价值，尤其连接肿块或致密结节影的牛角征更有特异性。
（7）塔尖征：癌瘤浸润淋巴管，致使淋巴管扩张及管内癌栓形成，从而可见一自肿块影向外笔直伸展的细条状致密影，状如塔尖。为乳腺癌的重要特征。
（8）乳房后间隙改变：深部乳腺癌可早期侵及浅筋膜的深层，导致乳房后间隙的透亮区消失。
（9）乳腺组织结构紊乱：不均匀低密度区及污秽的点片影。
（10）乳房形态改变：乳腺癌沿导管及腺体浸润时，尤其是向浅表浸润时，受累区膨出可致乳房变形。
（二）乳腺导管造影
乳腺导管造影不但可清晰显示乳腺导管及其细微结构，而且可以了解病变的部位及范围，弥补平片之不足，是早期发现微小癌的重要方法。对乳头溢液的良恶性乳腺疾病均有较大诊断价值。其主要用于不伴有乳房肿块的单个乳管呈血性、浆液性、水样乳头溢液者，或乳头溢液伴相应区域乳房包块诊断不明确者。
常见的乳腺导管造影恶性征象有：
1．导管本身因癌浸润、梗阻、破坏等引起的征象造影剂在大导管及二、三级分支表现为密度深浅不均，大小不一的“虫蚀征”；断续状分布的“断续征”；不规则充盈缺损；以及造景剂由导管破坏处向间质溢出形成大小不等之斑片状影的“潭湖征”。
2．因癌肿侵犯、收缩、压迫导管等引起的征象造影剂突然狭窄呈“鼠尾征”；一侧管壁僵直，突然中断等。亦可见虫蚀征。
（三）乳腺囊肿内充气造影
乳腺囊肿内充气造影主要用于临床与X线平片疑有乳腺囊性病变需确定性质，或疑有囊壁肿瘤需进一步确诊者。其恶生征象表现为：部分囊壁增厚，边缘不光整，甚至出现分叶状或毛刺状肿块等，则应首先考虑到癌变的可能。
二、超声检查
超声波检查对乳腺癌诊断准确率可达80%~85%，但对1cm以下者诊断准确率有待进一步提高。临床主要用于辅助X线检查之不足。
一般来说，恶性肿块边界不清，呈锯齿状，内部为低回声或强回声或不均匀回声，不同组织学类型的癌肿可使块后方回声增强或衰弱，肿块无滑动，无压缩，多数肿块长度大于深度。如皮肤局部回声线增厚、分层不清晰，乳头回缩，导管扩张，Cooper ′s韧带呈线性或三角形增厚，应高度重视有否早期乳癌。在恶性病变中，具有影像特征的如：①乳头状导管癌，乳头下方导管扩张呈分枝状，管内有强回声团突起。②硬癌，肿块不大，后方明显衰减。③髓样癌，呈球形，常为混合性回声，后方不衰减。
三、细胞学检查
细胞学检查包括：细钟吸取细胞学检查，乳头溢液涂片细胞学检查，乳头或肿瘤刮片细胞学检查及乳腺肿瘤切除标本印片细胞学检查。主要用于孤立病变，考虑为囊肿、良性或恶生肿瘤。临床明显的囊性病变、乳腺癌术后疤痕上孤立或多发的小结节、可疑的远处转移病灶、包括皮肤结节和肿大的淋巴结等可行诊断性穿刺。
四、活组织检查
用于乳腺诊断的活组织检查方法有切除活检、切取活检、穿刺活检、溃疡病灶的咬取活检、乳管内镜咬取活检等。
（一）切除活检
1．检查指征可触及的肿块，有痛性的肿块不能排除恶变者；非可及性肿块或X线上显示微小钙化；一个或两个乳管持续性自发性溢液；乳头的异常，乳头周围糜烂或近来自发性乳头回缩；乳腺皮肤的改变，如酒窝征、橘皮样变，或非炎症性皮肤改变；液窝淋巴结肿大；针吸细胞学检查阳性。
2．评价切除活检为临床常规方法，最为常用。既能达到活检的目的，又能达到治疗的目的，目前多主张此法。但冰冻检有时有假阳性或假阴性，应以否蜡活检为准。
（二）切取活检
1．检查指征基本同“切除活检”，适用于较大、已与皮肤粘连或已溃破的肿瘤。
2．评价切取活检有促进肿瘤转移的可能，除非肿瘤很大，尽量避免行切取活检。
（三）穿刺活检
1．检查指征乳房肿块考虑良性或恶性肿瘤；乳腺癌术后术区孤立或多发的小结节；可疑为转移的肿大淋巴结或皮肤结节，以及一切右通过穿刺取材部位的转移或可疑转移的病变。
2．评价易受穿刺针具和操作技术的影响，结果往往不十分可靠。操作时应避免造成肿瘤的播散。目前，利用高频X线电脑全自动定向活检装置，可对乳腺微小病变行准确定位，可望提高准确率。
（四）溃疡病灶咬取活检
适用于已破溃的肿瘤。一般在肿瘤破溃的边缘咬取部分进行肿瘤组织学检查及受体测定。取材时要避开坏死区，以免曩诊断，同时切忌挤压肿瘤组织。
（五）乳管内镜咬取活检
乳管内镜可确定病变的准确位置和性状，以及从乳管开口到病变部位的距离。此检查还可确认乳腺癌患侧乳管内的浸润情况，为施行保留乳头的乳腺癌根治术或保留乳房手术提供可靠依据。
五、热图检查
常用热图检查有液晶及远红外热图像两种方法。乳腺癌的热图像表现为：①局部放射热增加或出现热点；②局部血管增多或增粗、迂曲，可血管走向反常；③两侧温度明显不对称，患侧温度显著增高；④乳晕部热增加。但热图对较小肿瘤检出度低，假阳性及假阴性较多，经广泛评价后，目前大多已不将此法作为诊断乳腺癌而有明显异常温度记录者，可判断其预后较差。
六、近红外线乳腺扫描检查
乳腺癌的近红外线乳腺扫描图像表现为：限局性边缘不清的深灰或黑色的不均匀的吸光团，加压后不褪色（不发白），有时全乳呈深灰，需要增加探测器的亮度来得到与正常乳腺同机关报分辨率图像，周围有C型血管，双乳静脉系统的对称性消失，未受累乳腺呈正常表现，受累乳腺静脉扩张，呈广泛性扭曲和迂回，同时伴有静脉数量增加等。血管分型大多是VB4、VC2、VC3、VC4类型乳腺。液窝淋巴结呈现浅到深灰色卵圆形或圆形的均匀的灰色阴影。
乳腺癌近红外线图像有以下特点：①多级灰度倒环较多见，大部分为4级。②大多级倒环中3级灰度并不占据很大面积，点状和小片状3级灰度较多见。③在3级倒环周围，1~2级倒环面积较大，且分部不规则，尤其与中心的3级环无向心性分布。
近红外线检查对乳腺肿块诊断的准确率可达80%，且对乳腺充血性病变和血管的显示有一定特点，可作为一种辅助诊断方法。但对直径1cm以下的深部肿块易出现假阴性，宜与其他方法配合使用。
七、生物学标记检查
目前开展的生物学标记检查有癌胚抗原（CEA）、降钙素、含铁蛋白、单克隆抗体（CA15-3）等。生物学标记检查临床应用尚无足够的特异性和敏感性。应用多种标记物作为联合指标，可提高诊断价值，但亦只限于较晚期的乳腺癌病倒，对早期病倒亦无足够的敏感性。
八、PCR法癌基因诊断检查
K19和MUC1等检查与乳腺癌相关性较好，可检测出存在体内的微小转移灶。
九、激素受体检查
激素受体检查目前主要用于制订乳腺癌术后辅助治疗的方案及其预后的判断。目前用于临床的有：雌激素受体（ER）、孕激素受体（PR）检查。
十、其他检查
1．CT扫描CT扫描可用于不能扪及的乳腺病变组织检查前定位，确诊乳腺癌的手术前分期，检查乳腺后区、液部及内乳淋巴结有无肿大，有助于制订治疗计划。此法对纵隔、乳内淋巴结及胸骨病灶的诊断有极大的优势。但CT不是乳腺癌常规的诊断方法。
2．MRI MRI在鉴别良恶性病变，发现乳腺癌癌前病变可能有较大前景，但MRI不能显示微细钙化点，目前研究尚不能满足临床需要。
女性如何通过自查发现肿瘤？
一是观血。即阴道出血，如月经增多，周期紊乱，绝经后出血，接触性
出血等。常常由于宫颈或宫体发生肿瘤所致。当然，卵巢肿瘤也可因内分泌变化而表现月经紊乱和不正常出血。因此，除正常月经以外的出血都要究其原因后而对症诊治。
二是观带。女性白带是指各种质与量的阴道分泌物。正常的白带是少量的白色略显粘稠的分泌物，随着月经周期其量和稀薄度会有轻微变化。但脓性白带、血性白带、米泔样白带、水样白带等都是不正常的。除脓性白带之外，血性白带应注意宫颈肿瘤，晚期宫颈癌可有米泔样或淘米水样白带。
三是自摸肿块。当肿瘤很小时自己是摸不到的。自己能摸到肿瘤说明肿瘤已经相当大了。在清晨，空腹排解完大小便，平卧于床，略弯双膝，放松腹部，用双手在下腹部按触，由轻浅到重深，肿物是可以发现的。
四是感觉疼痛。下腹部、腰背部、骶尾部疼痛，性交痛等。疼痛并不是肿瘤的早期症状。通常当肿瘤体积相当大，压迫或侵犯其他脏器时，才会引起疼痛。有时疼痛也是肿瘤的自我暴露，如肿瘤发生蒂扭转，破裂或变性等都会引起腹部疼痛。
出血等。常常由于宫颈或宫体发生肿瘤所致。当然，卵巢肿瘤也可因内分泌变化而表现月经紊乱和不正常出血。因此，除正常月经以外的出血都要究其原因后而对症诊治。
二是观带。女性白带是指各种质与量的阴道分泌物。正常的白带是少量的白色略显粘稠的分泌物，随着月经周期其量和稀薄度会有轻微变化。但脓性白带、血性白带、米泔样白带、水样白带等都是不正常的。除脓性白带之外，血性白带应注意宫颈肿瘤，晚期宫颈癌可有米泔样或淘米水样白带。
三是自摸肿块。当肿瘤很小时自己是摸不到的。自己能摸到肿瘤说明肿瘤已经相当大了。在清晨，空腹排解完大小便，平卧于床，略弯双膝，放松腹部，用双手在下腹部按触，由轻浅到重深，肿物是可以发现的。
四是感觉疼痛。下腹部、腰背部、骶尾部疼痛，性交痛等。疼痛并不是肿瘤的早期症状。通常当肿瘤体积相当大，压迫或侵犯其他脏器时，才会引起疼痛。有时疼痛也是肿瘤的自我暴露，如肿瘤发生蒂扭转，破裂或变性等都会引起腹部疼痛。
癌症早期诊断方法——电脑的临床应用
现在已迈入电脑万能时代的说法并不为过。因此许多专家、学者正积极地研究，希望利用电脑的辅助早一天控制癌症。
有种称为电脑断层摄影的方法，在临床上已广为应用。这是利用Ｘ光详细做了断层摄影，再把资料输入于电脑存储、组合，如此来调查病变。这种方法，对脑肿瘤、肝癌、胰腺癌等等的脏器肿瘤的治疗发挥很大的功效，已经相当的实用化了。
对胃部的Ｘ光照片和电脑的配合使用也已被开发出来，Ｘ光胶卷上的银粒子接触到放射线即会黑色化。让电脑来阅读“银黑化粒子数”。如此即可轻易判断出是不是有癌症。
Ｘ光照片上的起伏形状，用肉眼无法辨别的隆起或凹陷部份等等。只要配合数张特殊照片就可利用电脑判断得更明确。这种研究目前正在逐渐进行中，从电脑的优秀性能来看，相信将来一定会有非凡的成就。
一提到电脑，人们就会想起癌病人的背部号码化。每年因癌症丧命的人逐渐增长，按照日本国内统计，一亿多人口的日本，在１９７７年度就有１４万人因癌症死亡。依此计算，每一位医师都能得到病人的资料，那么，理论上许多位医师都能得到病人的资料，那么，理论上许多位医师能够共同管理一位病人。
例如：某人患有胃病，到某医院就诊，此刻拍Ｘ光照片，做了各种详细检查，如此有了许多资料，再来诊断治疗，而且把这位病人的病暂时性治好；但是，经过数日或数年之后，胃部又不舒服，又到另一家医院就诊，同样又拍Ｘ光照片，做种种检查。倘若此刻只要轻按钮就可知道上次的病历资料，则可把两位医师的诊断结果相互比较，那么，更可详细了解病人的一切状况了。
人的记忆有限，所以把许多资料记忆让电脑来承担，如此就可把上次及这次或现在、将来调查的检查结果互相对照，这样也许能更快发现另一些疾病或癌也说不定。
但是，现在的医疗机构几乎与其他的医疗机构无联系性，每一家医院都独立地为病人治疗，在毫不了解以往的医师的判断治疗的情况下治疗。
同一家医院，往往也因为不同的医师而做不同的判断，倘若数位医师同时对一位病人来讨论治疗方针、诊断结论等等，相信一定能诊断得更正确。
让机械帮助人类记忆，新的资料也经过机械来处理判断。无论在何处诊断的资料，对同一疾病的病人，依背号的号码制度化来处理，则每位医师都能在不同之处了解病人的消息，也会知道两年前、三年前的病历。
随着科学技术的发达，电脑已经成为时代的宠儿，一个借助电脑进行诊断、早期发现癌症、帮助决定治疗方针的时代已经来临！
有种称为电脑断层摄影的方法，在临床上已广为应用。这是利用Ｘ光详细做了断层摄影，再把资料输入于电脑存储、组合，如此来调查病变。这种方法，对脑肿瘤、肝癌、胰腺癌等等的脏器肿瘤的治疗发挥很大的功效，已经相当的实用化了。
对胃部的Ｘ光照片和电脑的配合使用也已被开发出来，Ｘ光胶卷上的银粒子接触到放射线即会黑色化。让电脑来阅读“银黑化粒子数”。如此即可轻易判断出是不是有癌症。
Ｘ光照片上的起伏形状，用肉眼无法辨别的隆起或凹陷部份等等。只要配合数张特殊照片就可利用电脑判断得更明确。这种研究目前正在逐渐进行中，从电脑的优秀性能来看，相信将来一定会有非凡的成就。
一提到电脑，人们就会想起癌病人的背部号码化。每年因癌症丧命的人逐渐增长，按照日本国内统计，一亿多人口的日本，在１９７７年度就有１４万人因癌症死亡。依此计算，每一位医师都能得到病人的资料，那么，理论上许多位医师都能得到病人的资料，那么，理论上许多位医师能够共同管理一位病人。
例如：某人患有胃病，到某医院就诊，此刻拍Ｘ光照片，做了各种详细检查，如此有了许多资料，再来诊断治疗，而且把这位病人的病暂时性治好；但是，经过数日或数年之后，胃部又不舒服，又到另一家医院就诊，同样又拍Ｘ光照片，做种种检查。倘若此刻只要轻按钮就可知道上次的病历资料，则可把两位医师的诊断结果相互比较，那么，更可详细了解病人的一切状况了。
人的记忆有限，所以把许多资料记忆让电脑来承担，如此就可把上次及这次或现在、将来调查的检查结果互相对照，这样也许能更快发现另一些疾病或癌也说不定。
但是，现在的医疗机构几乎与其他的医疗机构无联系性，每一家医院都独立地为病人治疗，在毫不了解以往的医师的判断治疗的情况下治疗。
同一家医院，往往也因为不同的医师而做不同的判断，倘若数位医师同时对一位病人来讨论治疗方针、诊断结论等等，相信一定能诊断得更正确。
让机械帮助人类记忆，新的资料也经过机械来处理判断。无论在何处诊断的资料，对同一疾病的病人，依背号的号码制度化来处理，则每位医师都能在不同之处了解病人的消息，也会知道两年前、三年前的病历。
随着科学技术的发达，电脑已经成为时代的宠儿，一个借助电脑进行诊断、早期发现癌症、帮助决定治疗方针的时代已经来临！
FDG-PET有利于胆囊癌的鉴别诊断
采用氟18标记的脱氧葡萄糖正电子发射断层X线摄影（FDG-PET）对于胆囊癌的鉴别诊断能起到重要的辅助作用。
日本京都大学医学院的Koh T博士及其同事指出，胆囊癌的手术前鉴别诊断是普外科的一个难题，PET可能起到辅助作用。
研究人员选取16例发现胆囊突起性病变的患者，在手术前采用FDG-PET检测，以出现FDG局部聚集为恶性标准，并将结果与术后病理学结果进行比较。
结果发现，FDG-PET诊断胆囊癌的敏感性和特异性分别为75%和87.5%。2例患者出现假阴性，其中一例患有糖尿病，一例病变较小。另有1例黄色肉芽肿性胆囊炎患者出现假阳性。
Koh博士等认为，FDG-PET对于胆囊癌的鉴别诊断能起到重要的辅助作用。
日本京都大学医学院的Koh T博士及其同事指出，胆囊癌的手术前鉴别诊断是普外科的一个难题，PET可能起到辅助作用。
研究人员选取16例发现胆囊突起性病变的患者，在手术前采用FDG-PET检测，以出现FDG局部聚集为恶性标准，并将结果与术后病理学结果进行比较。
结果发现，FDG-PET诊断胆囊癌的敏感性和特异性分别为75%和87.5%。2例患者出现假阴性，其中一例患有糖尿病，一例病变较小。另有1例黄色肉芽肿性胆囊炎患者出现假阳性。
Koh博士等认为，FDG-PET对于胆囊癌的鉴别诊断能起到重要的辅助作用。
IV期肝门部胆管癌扩大肝切除的指征
在排除肝动脉和门静脉广泛侵犯后，IVA期肝门部胆管癌适于行根治性扩大肝切除术。但对于有远处转移和腹腔转移的IVB期患者，手术难以改善长期预后，支架植入是治疗首选。
日本和歌山医科大学的Uchiyama K博士及其同事指出，对于肝门部胆管癌，同时扩大肝切除和肝外胆道切除是唯一治愈的希望。但是IV期肿瘤患者是否适于扩大手术还存在争议。
研究人员选取1981年至2001年间接受治疗的肝门部胆管癌患者，进行回顾性研究。共有57名IVA和IVB期肿瘤患者，手术组33例接受扩大肝切除术，EMBS（自扩张金属胆道支架）组24例接受金属胆道支架植入。
结果发现，手术组的生存期为25.7±40.9个月，EMBS组为6.5±5.8个月（P=0.03）。手术组中21例患者（64%）达到根治，但在IVB期患者中，两组的生存期无显著差异。
Wakayama博士认为，IVA期肝门部胆管癌在排除肝动脉和门静脉广泛侵犯后，适于行根治性扩大肝切除术。但对于有远处转移和腹腔转移的IVB期患者，手术难以改善长期预后，支架植入应作为首选治疗。
日本和歌山医科大学的Uchiyama K博士及其同事指出，对于肝门部胆管癌，同时扩大肝切除和肝外胆道切除是唯一治愈的希望。但是IV期肿瘤患者是否适于扩大手术还存在争议。
研究人员选取1981年至2001年间接受治疗的肝门部胆管癌患者，进行回顾性研究。共有57名IVA和IVB期肿瘤患者，手术组33例接受扩大肝切除术，EMBS（自扩张金属胆道支架）组24例接受金属胆道支架植入。
结果发现，手术组的生存期为25.7±40.9个月，EMBS组为6.5±5.8个月（P=0.03）。手术组中21例患者（64%）达到根治，但在IVB期患者中，两组的生存期无显著差异。
Wakayama博士认为，IVA期肝门部胆管癌在排除肝动脉和门静脉广泛侵犯后，适于行根治性扩大肝切除术。但对于有远处转移和腹腔转移的IVB期患者，手术难以改善长期预后，支架植入应作为首选治疗。
七种常见食物助你快速消除口臭
这里说的除臭剂可别误会，是我们餐桌、厨房里常见的具有清除口臭作用的食物。
牛奶：
吃大蒜后的口气难闻，喝一杯牛奶，大蒜臭味即可消除。
柠檬：
性酸，味微苦，具有生津、止渴、祛暑的功效。可在一杯沸水里，加入一些薄荷，同时加上一些新鲜柠檬汁饮用，可去口臭。
柚子：
性酸，味寒，可治纳少、口淡，去胃中恶气，解酒毒，消除饮酒后口中异味，有消食健脾、芳香除臭的功效。取新鲜柚子去皮食肉，细细嚼服。
金橘：
性辛，味甘，具有理气解郁、化痰醒酒的功效。对口臭伴胸闷食滞很有效，可取新鲜金橘5—6枚，洗净嚼服。本方具有芳香通窍、顺气健脾的功效。
蜂蜜：
蜂蜜1匙，温开水1小杯冲服，每日晨起空腹即饮。蜂蜜具有润肠通腑、化消去腐的功效，对便秘引起的口臭颇有效。
山楂：
性酸，味微甘平，有散瘀消积、清胃、除口酸臭的功效。取山楂30枚，文火煨黄、煮汤，加冰糖少量，每次1小碗。
茶叶：
性苦，味寒，有止渴、清神、消食、除烦去腻的功效。用浓茶漱口或口嚼茶叶可除口臭。对进食大蒜、羊肉等食物后口气难闻，用茶叶1小撮，分次置于口中，慢嚼，待唾液化解茶叶后徐徐咽下，疗效颇佳。
牛奶：
吃大蒜后的口气难闻，喝一杯牛奶，大蒜臭味即可消除。
柠檬：
性酸，味微苦，具有生津、止渴、祛暑的功效。可在一杯沸水里，加入一些薄荷，同时加上一些新鲜柠檬汁饮用，可去口臭。
柚子：
性酸，味寒，可治纳少、口淡，去胃中恶气，解酒毒，消除饮酒后口中异味，有消食健脾、芳香除臭的功效。取新鲜柚子去皮食肉，细细嚼服。
金橘：
性辛，味甘，具有理气解郁、化痰醒酒的功效。对口臭伴胸闷食滞很有效，可取新鲜金橘5—6枚，洗净嚼服。本方具有芳香通窍、顺气健脾的功效。
蜂蜜：
蜂蜜1匙，温开水1小杯冲服，每日晨起空腹即饮。蜂蜜具有润肠通腑、化消去腐的功效，对便秘引起的口臭颇有效。
山楂：
性酸，味微甘平，有散瘀消积、清胃、除口酸臭的功效。取山楂30枚，文火煨黄、煮汤，加冰糖少量，每次1小碗。
茶叶：
性苦，味寒，有止渴、清神、消食、除烦去腻的功效。用浓茶漱口或口嚼茶叶可除口臭。对进食大蒜、羊肉等食物后口气难闻，用茶叶1小撮，分次置于口中，慢嚼，待唾液化解茶叶后徐徐咽下，疗效颇佳。
肿瘤病理诊断法和技术
肿瘤病理诊断最常用的方法是活体组织检查（简称活检）和脱落细胞学检查。活检是在病变部位用刀、钳等手术器具切取或钳取全部或部分肿瘤组织，也可用穿刺吸取肿瘤组织，然后制成病理组织切片在显微镜下观察，最后做出诊断。脱落细胞学检查是利用癌细胞之间粘附力，易随分泌物、排泄物（如痰液、乳头溢液、尿液等（自然脱落的特点，或医生用器械（如刮匙、食管拉网器等）将癌细胞从粘膜表面刮下来，制成涂片，用显微镜观察，做出细胞学诊断。
应用上述常用病理学检查方法，大多数肿瘤能获得明确诊断，但尚有8%~10%患者，尤其是分化差的肿瘤或涉及到该肿瘤的组织来源和功能状态时，难以确诊。随着现代科学技术包括免疫荧光和免疫组织化学、免疫电子显微镜、自动图象分析技术、流式细胞仪、细胞遗传学技术和原位分子杂交技术等。这些新技术的应用，无疑大大促进了肿瘤病理诊断和研究水平的提高，而且对肿瘤的组织来源、功能状态、发病机制的探讨，对肿瘤患者预后判断等提供了大量极有用的信息，为临床制订最佳治疗方案提供依据。
应用上述常用病理学检查方法，大多数肿瘤能获得明确诊断，但尚有8%~10%患者，尤其是分化差的肿瘤或涉及到该肿瘤的组织来源和功能状态时，难以确诊。随着现代科学技术包括免疫荧光和免疫组织化学、免疫电子显微镜、自动图象分析技术、流式细胞仪、细胞遗传学技术和原位分子杂交技术等。这些新技术的应用，无疑大大促进了肿瘤病理诊断和研究水平的提高，而且对肿瘤的组织来源、功能状态、发病机制的探讨，对肿瘤患者预后判断等提供了大量极有用的信息，为临床制订最佳治疗方案提供依据。
消化系统癌症预防侦测
从一九八二年起，癌症就跃居台湾地区十大死亡原因的第一位，且每年因癌症而死亡的人数仍不断增加，今天，台湾平均每四个人死亡，就有一位是由癌症所引起。因此如何预防癌症，如何在癌症发生的初期就发现它，使它不至于进展为末期癌，以挽救更多的生命，是非常重要的课题。
在十大恶性肿瘤的死因中，消化系统癌症占了三位，而且始终是排名在前六名以内，可见它的发生率颇高，它们分别是肝癌、大肠直肠癌与胃癌。兹分别介绍如下：
一、肝癌：
一九九七年统计资料中，肝癌是台湾地区癌症死因之第二位，由于台湾地区Ｂ型肝炎带原者有17%以上，台湾每年约有5000人死于肝癌。有些人比较容易发生肝癌，我们称这些人为高危险群患者，因为他们需要特别小心防范癌症的发生。这些人包括肝硬化、慢性Ｂ型肝炎或Ｃ型肝炎带原者，以及家族中有人得肝癌者。台湾地区肝癌患者80％-90％有Ｂ型肝炎带原，故Ｂ型肝炎是中国人肝癌最重要的致病因素，其发病年龄平均约在55岁。
而Ｃ型肝炎也是引起肝癌的原因之一。最近研究指出，Ｂ型肝炎表面抗原阴性之肝癌患者，65%有Ｃ肝炎，其发生肝癌平均年龄约在65岁。
初期肝癌几乎没有什么症状，故建议高危险人群患者应每四个月到医院追踪一次，抽血检验甲型胎儿蛋白和肝脏超声波扫描，若有怀疑罹病再进一步作血管摄影、电脑断层摄影或肝穿刺细胞学检查，以确定诊断。
由于医学进步，早期肝癌的治疗效果很好，有的肝癌可治愈，有的患者可延长多年寿命，主要的治疗方式有手术、血管栓塞与局部酒精注射，应与专科医师讨论，切勿迷信偏方，拖到末期不可收拾的地步才来就医。
台湾自一九八四年七月开始新生儿的Ｂ型肝炎疫苗接种计划，虽然用了大笔的经费，至今却证明是一个睿智的决策，不但将台湾下一代的Ｂ型肝炎带原者从17%减少到1%以下，而且也使下一代的肝硬化、肝癌患者减少到同先进国家相当，因此也节省了将来庞大的的医疗社会成本。
除新生儿接受Ｂ型肝炎疫苗接种外，避免不必要的打针、输血、针灸、刺青，避免酗酒及不食用不新鲜的花生或豆谷类（可能含黄麴毒素）是预防肝癌的方法。
二、胃癌：
胃癌在消化系统癌症中排名第二，仅次于肝癌。在所有恶性肿瘤的死因中，胃癌始终排名在前五名以内，可见它的发生率颇高。胃癌的成因中，饮食是最重要的因素，日本在胃癌方面的研究相当深入，其研究显示腌渍食物可能是造成胃癌的主因。其他高危险群计有萎缩性胃炎，恶性贫血，胃癌或大肠癌家族史，A型血型，曾经接受胃切除手术已超过十年以上者，吸烟者，低社会收入阶层者，及以前得过胃癌经过治疗后的患者。这些人得到胃癌的机率都比一般人略高，最近的研究也发现孩童时期胃内感染幽门杆菌可能会增加胃癌的机会。
一般而言，胃癌早期不一定有什么特别的症状，病人多半是因为上腹痛，腹部不适，或者因胃出血去医院照胃镜而意外发现的，因此很多人发现时已经是末期了。因为胃癌如果能早期发现，早期治疗，预后非常的好，而且再发率极低。所以如何早期发现胃癌是非常重要的常识。当患者属高危险群或50岁以上病人有疑似症状时（上腹痛，腹胀，食欲不振，贫血，吐血，解黑色大便，或是不明原因体重减轻时），就应该受胃镜或上消化道X光摄影检查，才能在早期便发现胃癌。
什么食物比较容易会造成胃癌？一般而言，腌渍或添加硝化防腐的肉类（肉干、火腿、香肠），醺烤的食物（尤其是烧焦的肉类），及吸烟、喝酒，都较容易促进胃癌的发生。反之食用牛奶和新鲜的蔬果则对胃有保护作用。美国在30年代发明冰箱之后胃癌的人数逐年减少，因为冰箱温度低，细菌不易滋长，较能保持食物的新鲜。因此不新鲜的食物，尤其是肉类，应该少吃，吃剩的食物一定要放冰箱，储存时间太久的食物应丢弃。
手术切除仍是目前治疗胃癌最主要的方法。另外少数早期胃癌患者，可尝试用内窥镜切除或局部激光治疗。早期胃癌手术治疗的成绩非常好，五年的存活率高达90%以上。至于晚期胃癌，手术加上辅助性化学治疗也可以达到20-40%的五年存活率，因此一旦诊断为胃癌，皆建议积极治疗。
三、大肠直肠癌：
50岁以上的患者如果有便血、大便习惯改变、贫血、肛门觉得粪便解不干净、腹部摸到硬块、或是不明原因体重减轻等现象，就应注意有大肠直肠癌的可能性。其高危险群包括大肠直肠癌家族史，大肠直肠癌术后患者，大肠曾发现息肉者，胃癌、甲状腺癌、乳癌患者，及溃疡性结肠炎患者。
除基因遗传的因素之外，大肠直肠癌与食物也有密切关系。现代人高脂肪、高胆固醇、高热量、以及低纤维的饮食习惯，正是大肠直肠癌病患日渐增多，且发病年龄逐年下降的原因之一。因为油脂会刺激胆汁大量分泌，而胆汁中的胆酸被肠道细菌分解产生致癌物，而且低纤维的食物容易造成便秘，使致癌物与肠壁接触时间延长，日积月累终于形成癌病灶。
若要早期发现大肠直肠癌，建议50岁以上的人们每年做一次大便潜血检查。
如果有大便习惯改变、肛门里急后重、或是不明原因体重减轻等现象，应尽早找专科医师讨论是否需作进一步检查。而高危险人群患者应每半年做一次便潜血检查，并到医院找专科医师安排一次大肠镜或大肠钡餐X光摄影检查，发现息肉则应立即切除。若检查正常，则须依医师建议日期定期追踪。
大肠直肠癌的预防方法，应尽量吃低脂食物，以植物油取代动物性脂肪，多吃高纤维食物（新鲜蔬果及胚芽米、糙米、全麦），少吃精致零食，少吃高热量甜食或油炸食物，并避免便秘超过3日以上。
其他消化系统相关癌症还有口咽癌、食道癌、胆囊癌、胰腺癌、胆管癌等。兹分别间介绍如下：
四、口咽癌：
口腔癌位居男性癌症死亡排名的第五位，发生与吃槟榔、吸烟、喝酒等有密切关系，据统计，百分之九十左右的口腔癌病人有嚼食槟榔的习惯，国人男性嚼食槟榔比率则高达百分之十六；随着吃槟榔人口的增加，预期口腔癌发生率将持续上升，故口腔癌之防治以减少吃槟榔人口为首要重点，而口腔癌的早期诊断及适当治疗，将可延长口腔癌患者的存活率。建议有槟榔、吸烟、喝酒习惯者应戒除，并定期至口腔科检查口腔。若有长期不愈的口腔溃疡或流血，则应尽快就医。
五、食道癌：
前苏联地区、中国、日本、中亚地区及南非人民是食道癌的好发地带，喝烈酒或吸烟的男性，低社会经济阶层，从事金属业，长期食道炎的病人是高危险群，好发于40岁以上，多数发现时已相当末期，不易治疗。其最重要的早期症狀是吞食时食物难以下咽，或吞食时有异物感或疼痛。高危险群一有怀疑就应检查，以免延误病情。
其他如胆囊癌、胰腺癌、胆管癌等皆不易早期发现，因为几乎没有症状，因此年纪大的人平时生活保养以及定期做健康检查是非常重要的。
由上文可知，饮食、生活习惯与癌症有非常密切的关系，尤其现代人的饮食过度精致，生活压力大，普遍缺乏运动及农药污染等问题，使癌变机会大大增加。因此，如能借改变饮食、生活习惯以增强可能之防癌能力，可减少相当多的癌症发生。
一、贮存与烹调：
中国人是非常重视吃的民族，在此先谈一些食物的防癌。老年人经历过战火与穷困，养成了不浪费食物的习惯，隔夜菜照吃，眼睛视力差了，食物发霉了可能看不见，味觉退化，吃到不新鲜食品也吃不出来，就会在不知不觉中吃到一些致癌物。因此，最好的方法便是一次买少一点食物，不要堆一大堆在家里发霉，而且少吃腌制、罐头食品。吃剩的食物一定要放冰箱，贮存时间太久的食物应丢弃。
肉类尽量少吃油炸的，如盐酥鸡、炸鸡、炸排骨等。因为高温使油脂在高温下分解，易产生致癌物质，而高温油炸使肉类蛋白质及氨基酸分解，产生胺类衍生物，也有造成试验动物产生肉瘤的报道。
以炭火烧烤肉类时，其中的油脂滴在炭火上，会产生有毒性的“多环芳羟”随烟熏挥发，又吸收回食物中，故吃炭烤肉鱼类时常有一种特殊风味，但此种化合物却是致癌物质，所以烤肉时时最好用锡箔纸包起来烤，肉与炭火也不要太接近，烧焦的部份不要吃。
花生、豆类、玉米等贮存在湿热环境中，易滋生细菌，而产生麴毒素，黄麴毒素是很强的致癌物，亚洲、非洲地区的肝癌常与之有关，因此食物要妥善贮存。
二、食品添加物：
制造香肠、腊肉、肉干、火腿、腌肉等肉类制品时，为了抑制细菌生长，同时增加肉类制品特有的红色，常添加硝酸盐亚硝酸盐（Nitrite、Nitrate）。此类保存剂是一种合法的添加物，在允许范围内使用对人体应不致构成威胁，但若商家不合规定过量添加，或长期大量吃此类肉品时，则会对人体产生危害。这是因为硝酸盐、亚硝酸盐在胃液中或与肠道中之细菌作用时，可与蛋白质的酸解物----胺相结合、而形成一种致癌物----酸胺类的化合物（Nitrosamines、Nitrosamides）。如果胃粘膜长期与此类化合物接触，可能引发胃内细胞突变，进而演变成癌症。但是如能同时吃下足够的维生素A与C时，则有抑制此种结合的作用。因此食用加工肉、鱼类食品时，能同时配合吃富含维生素A与C的蔬菜水果，将可减少致癌物产生的机会。反过来说，吃这类肉制品时如果同时食用养乐多、酸奶等富含酵母菌的食品，则形成硝酸胺类化合物的可能性反会增加。
另外，因为台湾的食品管理不如先进国家完善，民众常买到许多未经登记的加工食物，都含有成份不明的添加剂，许多路边摊的蜜饯，传统市场加着色剂的腌菜、罐头，漂白过的面，加硼砂的肉丸，一再回锅的热油所炸的食物，都应小心分辨再食用。东西好吃不一定健康，购买食物时应注意标示的日期及成份，并慎重选信誉良好的品牌，才不会误食致癌的添加剂。
三、环境污染物：
台湾地处亚热带，为避免虫害，农药之使用量相当大，这些农药及化肥容易残留在新鲜蔬果表面上，食用宜清洗干净。此外畜牧业者在鸡、鸭、猪等身上注射促进生长的荷尔蒙以缩短生产周期，并为避免禽畜集体感染而过量使用抗生素，这些物质皆容易残存于肉品，尤其是内脏中，都对身体有不良的影响。
四、饮食及生活习惯：
未加工之豆类、高纤维食物如全麦、糙米以及五谷杂粮根茎类、及新鲜的蔬菜、水果都富含纤维质，能促进肠道蠕动，并刺激便快速排出，减少致癌物与肠道接触的时间，并冲淡肠道内致癌物质的浓度，因此纤维質摄取多的人们得癌的机会比较低。此外研究亦发现自然界中有多种食物可减少癌症机会，如：十字花科食物（青花菜、花椰菜、芥蓝菜、芥菜、高丽菜、青江菜、甘蓝菜、小白菜、白萝卜等）及含硫之食物（洋葱、大蒜）等，这些蔬菜可以多吃。
经常应酬者饮食过量，脂肪、热量摄取过多造成肥胖，与结肠癌、乳癌及其他之多种癌症有关。吃太多的肉类，摄取过量动物性脂肪，同时蔬菜水果却又吃得太少，酗酒吸烟又没运动，这些都大大增加了癌症发生的机会。
一般40岁以上的民众应可考虑定期作健康检查或防癌筛检。筛检之项目一般包括胃镜检查（或上消化道X光摄影）、女性子宫颈抹片检查、乳房检查、大肠X光摄影检查加上直肠镜检查（或大肠镜检查），肝脏部位超声波检查……至于高危险群，则必须针对可能罹患的癌病及早作防癌筛检。早期发现癌症是防癌工作的另一重点，借由筛检，可于癌症发生初期即诊断出来，预后多半很好。
最后，圣经说：“喜乐的心乃是良药，忧伤的灵使骨枯干。”一个人的心情若常保持轻松愉快，则他的自律神经、内分泌系统及免疫系统都会运作正常，自然不易得癌症。因此，培养积极乐观的人生观，适度休息，享受各样美善的事物，行善助人，将会使身体心灵都健康美好。
在十大恶性肿瘤的死因中，消化系统癌症占了三位，而且始终是排名在前六名以内，可见它的发生率颇高，它们分别是肝癌、大肠直肠癌与胃癌。兹分别介绍如下：
一、肝癌：
一九九七年统计资料中，肝癌是台湾地区癌症死因之第二位，由于台湾地区Ｂ型肝炎带原者有17%以上，台湾每年约有5000人死于肝癌。有些人比较容易发生肝癌，我们称这些人为高危险群患者，因为他们需要特别小心防范癌症的发生。这些人包括肝硬化、慢性Ｂ型肝炎或Ｃ型肝炎带原者，以及家族中有人得肝癌者。台湾地区肝癌患者80％-90％有Ｂ型肝炎带原，故Ｂ型肝炎是中国人肝癌最重要的致病因素，其发病年龄平均约在55岁。
而Ｃ型肝炎也是引起肝癌的原因之一。最近研究指出，Ｂ型肝炎表面抗原阴性之肝癌患者，65%有Ｃ肝炎，其发生肝癌平均年龄约在65岁。
初期肝癌几乎没有什么症状，故建议高危险人群患者应每四个月到医院追踪一次，抽血检验甲型胎儿蛋白和肝脏超声波扫描，若有怀疑罹病再进一步作血管摄影、电脑断层摄影或肝穿刺细胞学检查，以确定诊断。
由于医学进步，早期肝癌的治疗效果很好，有的肝癌可治愈，有的患者可延长多年寿命，主要的治疗方式有手术、血管栓塞与局部酒精注射，应与专科医师讨论，切勿迷信偏方，拖到末期不可收拾的地步才来就医。
台湾自一九八四年七月开始新生儿的Ｂ型肝炎疫苗接种计划，虽然用了大笔的经费，至今却证明是一个睿智的决策，不但将台湾下一代的Ｂ型肝炎带原者从17%减少到1%以下，而且也使下一代的肝硬化、肝癌患者减少到同先进国家相当，因此也节省了将来庞大的的医疗社会成本。
除新生儿接受Ｂ型肝炎疫苗接种外，避免不必要的打针、输血、针灸、刺青，避免酗酒及不食用不新鲜的花生或豆谷类（可能含黄麴毒素）是预防肝癌的方法。
二、胃癌：
胃癌在消化系统癌症中排名第二，仅次于肝癌。在所有恶性肿瘤的死因中，胃癌始终排名在前五名以内，可见它的发生率颇高。胃癌的成因中，饮食是最重要的因素，日本在胃癌方面的研究相当深入，其研究显示腌渍食物可能是造成胃癌的主因。其他高危险群计有萎缩性胃炎，恶性贫血，胃癌或大肠癌家族史，A型血型，曾经接受胃切除手术已超过十年以上者，吸烟者，低社会收入阶层者，及以前得过胃癌经过治疗后的患者。这些人得到胃癌的机率都比一般人略高，最近的研究也发现孩童时期胃内感染幽门杆菌可能会增加胃癌的机会。
一般而言，胃癌早期不一定有什么特别的症状，病人多半是因为上腹痛，腹部不适，或者因胃出血去医院照胃镜而意外发现的，因此很多人发现时已经是末期了。因为胃癌如果能早期发现，早期治疗，预后非常的好，而且再发率极低。所以如何早期发现胃癌是非常重要的常识。当患者属高危险群或50岁以上病人有疑似症状时（上腹痛，腹胀，食欲不振，贫血，吐血，解黑色大便，或是不明原因体重减轻时），就应该受胃镜或上消化道X光摄影检查，才能在早期便发现胃癌。
什么食物比较容易会造成胃癌？一般而言，腌渍或添加硝化防腐的肉类（肉干、火腿、香肠），醺烤的食物（尤其是烧焦的肉类），及吸烟、喝酒，都较容易促进胃癌的发生。反之食用牛奶和新鲜的蔬果则对胃有保护作用。美国在30年代发明冰箱之后胃癌的人数逐年减少，因为冰箱温度低，细菌不易滋长，较能保持食物的新鲜。因此不新鲜的食物，尤其是肉类，应该少吃，吃剩的食物一定要放冰箱，储存时间太久的食物应丢弃。
手术切除仍是目前治疗胃癌最主要的方法。另外少数早期胃癌患者，可尝试用内窥镜切除或局部激光治疗。早期胃癌手术治疗的成绩非常好，五年的存活率高达90%以上。至于晚期胃癌，手术加上辅助性化学治疗也可以达到20-40%的五年存活率，因此一旦诊断为胃癌，皆建议积极治疗。
三、大肠直肠癌：
50岁以上的患者如果有便血、大便习惯改变、贫血、肛门觉得粪便解不干净、腹部摸到硬块、或是不明原因体重减轻等现象，就应注意有大肠直肠癌的可能性。其高危险群包括大肠直肠癌家族史，大肠直肠癌术后患者，大肠曾发现息肉者，胃癌、甲状腺癌、乳癌患者，及溃疡性结肠炎患者。
除基因遗传的因素之外，大肠直肠癌与食物也有密切关系。现代人高脂肪、高胆固醇、高热量、以及低纤维的饮食习惯，正是大肠直肠癌病患日渐增多，且发病年龄逐年下降的原因之一。因为油脂会刺激胆汁大量分泌，而胆汁中的胆酸被肠道细菌分解产生致癌物，而且低纤维的食物容易造成便秘，使致癌物与肠壁接触时间延长，日积月累终于形成癌病灶。
若要早期发现大肠直肠癌，建议50岁以上的人们每年做一次大便潜血检查。
如果有大便习惯改变、肛门里急后重、或是不明原因体重减轻等现象，应尽早找专科医师讨论是否需作进一步检查。而高危险人群患者应每半年做一次便潜血检查，并到医院找专科医师安排一次大肠镜或大肠钡餐X光摄影检查，发现息肉则应立即切除。若检查正常，则须依医师建议日期定期追踪。
大肠直肠癌的预防方法，应尽量吃低脂食物，以植物油取代动物性脂肪，多吃高纤维食物（新鲜蔬果及胚芽米、糙米、全麦），少吃精致零食，少吃高热量甜食或油炸食物，并避免便秘超过3日以上。
其他消化系统相关癌症还有口咽癌、食道癌、胆囊癌、胰腺癌、胆管癌等。兹分别间介绍如下：
四、口咽癌：
口腔癌位居男性癌症死亡排名的第五位，发生与吃槟榔、吸烟、喝酒等有密切关系，据统计，百分之九十左右的口腔癌病人有嚼食槟榔的习惯，国人男性嚼食槟榔比率则高达百分之十六；随着吃槟榔人口的增加，预期口腔癌发生率将持续上升，故口腔癌之防治以减少吃槟榔人口为首要重点，而口腔癌的早期诊断及适当治疗，将可延长口腔癌患者的存活率。建议有槟榔、吸烟、喝酒习惯者应戒除，并定期至口腔科检查口腔。若有长期不愈的口腔溃疡或流血，则应尽快就医。
五、食道癌：
前苏联地区、中国、日本、中亚地区及南非人民是食道癌的好发地带，喝烈酒或吸烟的男性，低社会经济阶层，从事金属业，长期食道炎的病人是高危险群，好发于40岁以上，多数发现时已相当末期，不易治疗。其最重要的早期症狀是吞食时食物难以下咽，或吞食时有异物感或疼痛。高危险群一有怀疑就应检查，以免延误病情。
其他如胆囊癌、胰腺癌、胆管癌等皆不易早期发现，因为几乎没有症状，因此年纪大的人平时生活保养以及定期做健康检查是非常重要的。
由上文可知，饮食、生活习惯与癌症有非常密切的关系，尤其现代人的饮食过度精致，生活压力大，普遍缺乏运动及农药污染等问题，使癌变机会大大增加。因此，如能借改变饮食、生活习惯以增强可能之防癌能力，可减少相当多的癌症发生。
一、贮存与烹调：
中国人是非常重视吃的民族，在此先谈一些食物的防癌。老年人经历过战火与穷困，养成了不浪费食物的习惯，隔夜菜照吃，眼睛视力差了，食物发霉了可能看不见，味觉退化，吃到不新鲜食品也吃不出来，就会在不知不觉中吃到一些致癌物。因此，最好的方法便是一次买少一点食物，不要堆一大堆在家里发霉，而且少吃腌制、罐头食品。吃剩的食物一定要放冰箱，贮存时间太久的食物应丢弃。
肉类尽量少吃油炸的，如盐酥鸡、炸鸡、炸排骨等。因为高温使油脂在高温下分解，易产生致癌物质，而高温油炸使肉类蛋白质及氨基酸分解，产生胺类衍生物，也有造成试验动物产生肉瘤的报道。
以炭火烧烤肉类时，其中的油脂滴在炭火上，会产生有毒性的“多环芳羟”随烟熏挥发，又吸收回食物中，故吃炭烤肉鱼类时常有一种特殊风味，但此种化合物却是致癌物质，所以烤肉时时最好用锡箔纸包起来烤，肉与炭火也不要太接近，烧焦的部份不要吃。
花生、豆类、玉米等贮存在湿热环境中，易滋生细菌，而产生麴毒素，黄麴毒素是很强的致癌物，亚洲、非洲地区的肝癌常与之有关，因此食物要妥善贮存。
二、食品添加物：
制造香肠、腊肉、肉干、火腿、腌肉等肉类制品时，为了抑制细菌生长，同时增加肉类制品特有的红色，常添加硝酸盐亚硝酸盐（Nitrite、Nitrate）。此类保存剂是一种合法的添加物，在允许范围内使用对人体应不致构成威胁，但若商家不合规定过量添加，或长期大量吃此类肉品时，则会对人体产生危害。这是因为硝酸盐、亚硝酸盐在胃液中或与肠道中之细菌作用时，可与蛋白质的酸解物----胺相结合、而形成一种致癌物----酸胺类的化合物（Nitrosamines、Nitrosamides）。如果胃粘膜长期与此类化合物接触，可能引发胃内细胞突变，进而演变成癌症。但是如能同时吃下足够的维生素A与C时，则有抑制此种结合的作用。因此食用加工肉、鱼类食品时，能同时配合吃富含维生素A与C的蔬菜水果，将可减少致癌物产生的机会。反过来说，吃这类肉制品时如果同时食用养乐多、酸奶等富含酵母菌的食品，则形成硝酸胺类化合物的可能性反会增加。
另外，因为台湾的食品管理不如先进国家完善，民众常买到许多未经登记的加工食物，都含有成份不明的添加剂，许多路边摊的蜜饯，传统市场加着色剂的腌菜、罐头，漂白过的面，加硼砂的肉丸，一再回锅的热油所炸的食物，都应小心分辨再食用。东西好吃不一定健康，购买食物时应注意标示的日期及成份，并慎重选信誉良好的品牌，才不会误食致癌的添加剂。
三、环境污染物：
台湾地处亚热带，为避免虫害，农药之使用量相当大，这些农药及化肥容易残留在新鲜蔬果表面上，食用宜清洗干净。此外畜牧业者在鸡、鸭、猪等身上注射促进生长的荷尔蒙以缩短生产周期，并为避免禽畜集体感染而过量使用抗生素，这些物质皆容易残存于肉品，尤其是内脏中，都对身体有不良的影响。
四、饮食及生活习惯：
未加工之豆类、高纤维食物如全麦、糙米以及五谷杂粮根茎类、及新鲜的蔬菜、水果都富含纤维质，能促进肠道蠕动，并刺激便快速排出，减少致癌物与肠道接触的时间，并冲淡肠道内致癌物质的浓度，因此纤维質摄取多的人们得癌的机会比较低。此外研究亦发现自然界中有多种食物可减少癌症机会，如：十字花科食物（青花菜、花椰菜、芥蓝菜、芥菜、高丽菜、青江菜、甘蓝菜、小白菜、白萝卜等）及含硫之食物（洋葱、大蒜）等，这些蔬菜可以多吃。
经常应酬者饮食过量，脂肪、热量摄取过多造成肥胖，与结肠癌、乳癌及其他之多种癌症有关。吃太多的肉类，摄取过量动物性脂肪，同时蔬菜水果却又吃得太少，酗酒吸烟又没运动，这些都大大增加了癌症发生的机会。
一般40岁以上的民众应可考虑定期作健康检查或防癌筛检。筛检之项目一般包括胃镜检查（或上消化道X光摄影）、女性子宫颈抹片检查、乳房检查、大肠X光摄影检查加上直肠镜检查（或大肠镜检查），肝脏部位超声波检查……至于高危险群，则必须针对可能罹患的癌病及早作防癌筛检。早期发现癌症是防癌工作的另一重点，借由筛检，可于癌症发生初期即诊断出来，预后多半很好。
最后，圣经说：“喜乐的心乃是良药，忧伤的灵使骨枯干。”一个人的心情若常保持轻松愉快，则他的自律神经、内分泌系统及免疫系统都会运作正常，自然不易得癌症。因此，培养积极乐观的人生观，适度休息，享受各样美善的事物，行善助人，将会使身体心灵都健康美好。
晚期恶性肿瘤病人的主要症状
晚期恶性肿瘤患者，除肿瘤自身症状加重以外，还主要伴随以下四种症状：
一、发热：其病因繁多，如细菌、病毒的感染，结缔组织病，还有功能性发热。
二、疼痛：当正常组织收到肿瘤的破坏和浸润，导致对邻近的神经根受到压迫和破坏，局部组织缺血坏死，血液回流受阻，骨与骨膜受到浸润均可引起疼痛。因此，疼痛是晚期恶性肿瘤患者最常见的伴发症状。因此世界卫生组织制定的目标，要求在20世纪解决晚期恶性肿瘤患者的疼痛问题，但至今尚未寻找到真正的解决途径。目前采用的办法主要还是用镇痛剂和麻醉剂。
三、恶病质：是特指晚期肿瘤患者出现的极度消瘦、精神萎糜、体力虚衰。原因有三：
1、癌本身是一种慢性消耗性疾病，由于癌细胞异常而迅速的增殖，致使肿瘤患者对营养的需要比正常人要高，从而影响身体其他器官的功能。
2、癌症本身产生的毒性物质引起病人胃肠道功能紊乱，而出现恶心、呕吐、发热、食欲下降、体重减轻、日趋消瘦等，也影响机体功能。
3、癌症压迫或侵犯到邻近重要脏器，从而影响个体某组织器官的生理解剖功能。
四、恶性腔内积液：恶性腔内积液是恶性肿瘤的重要并发症，在临床上并不少见。但如处理不当可致迅速恶化以致死亡。发生恶性腔内积液的部位有胸腹腔、腹膜腔、心包腔等。胸腔内恶性积液约占胸腔积液的1/4左右，引起胸腔恶性积液的肿瘤有：肺癌、乳腺癌、胸膛间皮瘤、恶性淋巴瘤和卵巢癌等。其中乳癌恶性胸腔积液的发病率可能最高，约50%乳癌病人会因转移而引起恶性胸腔积液。肺癌次之，约28%病例发生胸水，其中以腺癌的发病率为最高，约为37%左右。胸膜间皮瘤的发病率较低，但本病并发恶性胸腔积液的很多。大量的胸腔恶性积液可以压迫肺组织，使肺容量降低，尤其是右肺（占呼吸功能的2/3以上），被胸水压迫后，引起呼吸功能障碍更大，会引起肺不张和肺部因引流不畅而致的感染。
一、发热：其病因繁多，如细菌、病毒的感染，结缔组织病，还有功能性发热。
二、疼痛：当正常组织收到肿瘤的破坏和浸润，导致对邻近的神经根受到压迫和破坏，局部组织缺血坏死，血液回流受阻，骨与骨膜受到浸润均可引起疼痛。因此，疼痛是晚期恶性肿瘤患者最常见的伴发症状。因此世界卫生组织制定的目标，要求在20世纪解决晚期恶性肿瘤患者的疼痛问题，但至今尚未寻找到真正的解决途径。目前采用的办法主要还是用镇痛剂和麻醉剂。
三、恶病质：是特指晚期肿瘤患者出现的极度消瘦、精神萎糜、体力虚衰。原因有三：
1、癌本身是一种慢性消耗性疾病，由于癌细胞异常而迅速的增殖，致使肿瘤患者对营养的需要比正常人要高，从而影响身体其他器官的功能。
2、癌症本身产生的毒性物质引起病人胃肠道功能紊乱，而出现恶心、呕吐、发热、食欲下降、体重减轻、日趋消瘦等，也影响机体功能。
3、癌症压迫或侵犯到邻近重要脏器，从而影响个体某组织器官的生理解剖功能。
四、恶性腔内积液：恶性腔内积液是恶性肿瘤的重要并发症，在临床上并不少见。但如处理不当可致迅速恶化以致死亡。发生恶性腔内积液的部位有胸腹腔、腹膜腔、心包腔等。胸腔内恶性积液约占胸腔积液的1/4左右，引起胸腔恶性积液的肿瘤有：肺癌、乳腺癌、胸膛间皮瘤、恶性淋巴瘤和卵巢癌等。其中乳癌恶性胸腔积液的发病率可能最高，约50%乳癌病人会因转移而引起恶性胸腔积液。肺癌次之，约28%病例发生胸水，其中以腺癌的发病率为最高，约为37%左右。胸膜间皮瘤的发病率较低，但本病并发恶性胸腔积液的很多。大量的胸腔恶性积液可以压迫肺组织，使肺容量降低，尤其是右肺（占呼吸功能的2/3以上），被胸水压迫后，引起呼吸功能障碍更大，会引起肺不张和肺部因引流不畅而致的感染。
儿童及青春期癌症有现状
德国明斯特大学儿童医院Jürgens1在欧洲肿瘤学会议上报告，儿童和青春期癌症发病率以人口为基础的癌症登记处记录显示，15岁以下新病例约14/10万儿童。5岁以内发病率是5岁以上者的2倍，男孩比女孩更受影响。全身性癌症与恶性实体肿瘤同样常见。主要的全身性肿瘤是儿童急性淋巴细胞白血病（约30％）、其次为急性粒细胞白血病（5％）、慢性粒细胞白血病（0.5％）。非霍奇金淋巴瘤要比霍奇金淋巴瘤
更常见。
最常见的实体瘤多发生在中枢神经系统（＞20％），如星形细胞瘤、成神经管细胞瘤、室管膜细胞瘤。常见的外周实体肿瘤是成神经细胞瘤(9％)、肾母细胞瘤(7％)、软组织肉瘤（7％,主要为横纹肌肉瘤）和骨肿瘤（5％,主要为骨肉瘤和Ewing瘤），其次为生殖细胞瘤(3％)、成视网膜细胞瘤（2％）。癌症可解释不到1％的儿童恶性肿瘤。诊断的分布在0～10岁与10～20岁患儿的肿瘤显著不同。所有“母细胞瘤”主要发生在5岁内，以后罕见。急性成淋巴细胞白血病在学龄前达到高峰发病率，以后进入平台期。淋巴瘤随年龄发病率增加，在5岁以下罕有发生。骨肿瘤主要发生在20～30岁，然而，横纹肌肉瘤和生殖细胞肿瘤表现为双相发病率。
儿童恶性肿瘤治疗手段包括化疗、放疗和手术治疗。全球5年生存率为76％，大多数为肉瘤约占60％，白血病和淋巴瘤为80％～90％（急性淋巴细胞白血病为84％，急性粒细胞白血病为48％），肾母细胞瘤和生殖细胞肿瘤为90％。虽然这种治疗使生存率和治愈率高，但晚期后遗症包括不育、损害心肾功能，引发第二种恶性肿瘤（20年后约5％）是显著的。
更常见。
最常见的实体瘤多发生在中枢神经系统（＞20％），如星形细胞瘤、成神经管细胞瘤、室管膜细胞瘤。常见的外周实体肿瘤是成神经细胞瘤(9％)、肾母细胞瘤(7％)、软组织肉瘤（7％,主要为横纹肌肉瘤）和骨肿瘤（5％,主要为骨肉瘤和Ewing瘤），其次为生殖细胞瘤(3％)、成视网膜细胞瘤（2％）。癌症可解释不到1％的儿童恶性肿瘤。诊断的分布在0～10岁与10～20岁患儿的肿瘤显著不同。所有“母细胞瘤”主要发生在5岁内，以后罕见。急性成淋巴细胞白血病在学龄前达到高峰发病率，以后进入平台期。淋巴瘤随年龄发病率增加，在5岁以下罕有发生。骨肿瘤主要发生在20～30岁，然而，横纹肌肉瘤和生殖细胞肿瘤表现为双相发病率。
儿童恶性肿瘤治疗手段包括化疗、放疗和手术治疗。全球5年生存率为76％，大多数为肉瘤约占60％，白血病和淋巴瘤为80％～90％（急性淋巴细胞白血病为84％，急性粒细胞白血病为48％），肾母细胞瘤和生殖细胞肿瘤为90％。虽然这种治疗使生存率和治愈率高，但晚期后遗症包括不育、损害心肾功能，引发第二种恶性肿瘤（20年后约5％）是显著的。
哪些病因会引起肿瘤
肿瘤的病因十分复杂，外界环境中各种刺激因素和机体内部某些潜在因素等多种因素相互作用，可引起原癌基因活化成为癌基因和（或）抑癌基因失活，从而导致肿瘤的发生。当今世界各国癌症绝对发病率的增高，在很大程度上与环境中的各种致癌因素有关。
迄今为止，动物实验证明化学致癌物已逾千种，与人类癌症密切有关者有30多种。烟草的烟雾，烟熏和烧烤食品中含有多环芳烃，与肺癌和胃癌发生有关。芳香胺类如乙嗪胺、联苯胺等，与印染工人和橡胶工人的膀胱癌发生有关。食品添加剂如奶油黄等，在动物实验中可引起大白鼠发生肝癌。霉变的食品中黄曲霉素B1可诱发肝癌。食品中亚硝胺含量高可诱发胃癌和食管癌。
电离辐射（X线、放射性核素）、紫外线、热辐射和异物等物理因素也可以诱发癌症。第二次世界大战时，日本长崎和广岛受原子弹爆炸影响的幸存居民中，白血病发病率明显增高，肺癌、甲状腺癌和乳腺癌等的发病率亦较高。日光中紫外线长期过度照射可引起皮肤癌。
1908年，有学者证明鸡白血病可以由不含细胞的滤液中一种因子引起，现已知这种滤过性因子就是病毒。1947年，有学者在罗斯肉瘤细胞中观察到病毒颗粒，称为罗斯肉瘤病毒，这是经过证实的第一株动物肿瘤病毒。目前已发现600多种动物肿瘤病毒，其中2/3为RNA病毒，1/3为DNA病毒。前者主要引起白血病和淋巴瘤，以及一小部分小鼠乳腺癌；后者包括乳头状瘤病毒、多瘤病毒、腺病毒和疱疹病毒等，可引起多种肿瘤。
在人类，已知Ⅰ型人T细胞白血病病毒（HTLV-I）与成人T细胞淋巴瘤（白血病）有关；某些亚型乳头状瘤病毒和疱疹病毒与子宫颈癌有关；乙型肝炎病毒与肝癌有关；EB病毒与鼻咽癌及某些类型淋巴瘤（伯基特淋巴瘤、霍奇金病、NK/T细胞淋巴瘤）有关。除病毒外，某些寄生虫也与癌症发生有关，例如日本血吸虫与结肠癌、埃及血吸虫与膀胱癌、中华支睾吸虫与胆管细胞癌均有一定的关系。
除了环境因素外，某些内在因素与人类某些癌症的发生有关，包括遗传因素、性别和年龄因素、种族因素、内分泌因素和机体免疫状态因素等。
迄今为止，动物实验证明化学致癌物已逾千种，与人类癌症密切有关者有30多种。烟草的烟雾，烟熏和烧烤食品中含有多环芳烃，与肺癌和胃癌发生有关。芳香胺类如乙嗪胺、联苯胺等，与印染工人和橡胶工人的膀胱癌发生有关。食品添加剂如奶油黄等，在动物实验中可引起大白鼠发生肝癌。霉变的食品中黄曲霉素B1可诱发肝癌。食品中亚硝胺含量高可诱发胃癌和食管癌。
电离辐射（X线、放射性核素）、紫外线、热辐射和异物等物理因素也可以诱发癌症。第二次世界大战时，日本长崎和广岛受原子弹爆炸影响的幸存居民中，白血病发病率明显增高，肺癌、甲状腺癌和乳腺癌等的发病率亦较高。日光中紫外线长期过度照射可引起皮肤癌。
1908年，有学者证明鸡白血病可以由不含细胞的滤液中一种因子引起，现已知这种滤过性因子就是病毒。1947年，有学者在罗斯肉瘤细胞中观察到病毒颗粒，称为罗斯肉瘤病毒，这是经过证实的第一株动物肿瘤病毒。目前已发现600多种动物肿瘤病毒，其中2/3为RNA病毒，1/3为DNA病毒。前者主要引起白血病和淋巴瘤，以及一小部分小鼠乳腺癌；后者包括乳头状瘤病毒、多瘤病毒、腺病毒和疱疹病毒等，可引起多种肿瘤。
在人类，已知Ⅰ型人T细胞白血病病毒（HTLV-I）与成人T细胞淋巴瘤（白血病）有关；某些亚型乳头状瘤病毒和疱疹病毒与子宫颈癌有关；乙型肝炎病毒与肝癌有关；EB病毒与鼻咽癌及某些类型淋巴瘤（伯基特淋巴瘤、霍奇金病、NK/T细胞淋巴瘤）有关。除病毒外，某些寄生虫也与癌症发生有关，例如日本血吸虫与结肠癌、埃及血吸虫与膀胱癌、中华支睾吸虫与胆管细胞癌均有一定的关系。
除了环境因素外，某些内在因素与人类某些癌症的发生有关，包括遗传因素、性别和年龄因素、种族因素、内分泌因素和机体免疫状态因素等。
癌症检查常用的方法有哪些？
癌症的检查，除了病人的自我检查以及医生的视、触、叩、听等一般检查之外，临床上还需进行实验室检查、放射学检查、放射性核素检查、超声波检查、内窥镜检查、手术探查等特殊检查。
1.实验室检查：主要包括血、尿、大便的常规检查、生化及免疫检查，病理学检查等。
2.放射学检查：主要包括X光透视、X光摄片、X光造影检查、CT扫描、核磁共振成像等。
3.放射性核素检查：即同位素检查，包括功能测定检查、扫描及伽玛照射检查、放射免疫分析等。
4.超声波检查：包括A型、B型超声波检查。
5.内窥镜检查：包括各种硬性或光学纤维镜、如喉镜、支气管镜、纵隔镜、食管镜、胃镜、胃十二指肠镜、结肠镜、直肠镜、肛门镜、膀胱镜、输尿管镜、肾镜、阴道镜、子宫镜等。
1.实验室检查：主要包括血、尿、大便的常规检查、生化及免疫检查，病理学检查等。
2.放射学检查：主要包括X光透视、X光摄片、X光造影检查、CT扫描、核磁共振成像等。
3.放射性核素检查：即同位素检查，包括功能测定检查、扫描及伽玛照射检查、放射免疫分析等。
4.超声波检查：包括A型、B型超声波检查。
5.内窥镜检查：包括各种硬性或光学纤维镜、如喉镜、支气管镜、纵隔镜、食管镜、胃镜、胃十二指肠镜、结肠镜、直肠镜、肛门镜、膀胱镜、输尿管镜、肾镜、阴道镜、子宫镜等。
2009年1月10日星期六
Uterine/Endometrial Cancer
WHAT IS UTERINE / ENDOMETRIAL CANCER?
Endometrial cancer is a disease in which malignant (cancer) cells form in the tissues of the endometrium.
The endometrium is the lining of the uterus. The uterus is a hollow, muscular organ in a woman’s pelvis. The uterus is where a fetus grows. In most nonpregnant women, the uterus is about 3 inches long.
Cancer of the endometrium is different from cancer of the muscle of the uterus, which is called sarcoma of the uterus. Cancer of the endometrium is the most common gynecologic malignancy and accounts for 6% of all cancers in women. It is a highly curable tumor.
Cellular Classification
The most common endometrial cancer cell type is endometrioid adenocarcinoma, which is composed of malignant glandular epithelial elements; an admixture of squamous metaplasia is not uncommon. Adenosquamous tumors contain malignant elements of both glandular and squamous epithelium; clear cell and papillary serous carcinoma of the endometrium are tumors that are histologically similar to those noted in the ovary and the fallopian tube, and the prognosis is worse for these tumors. Mucinous, squamous, and undifferentiated tumors are rarely encountered. Frequency of endometrial cancer cell types is as follows:
Endometrioid (75%-80%)
Ciliated adenocarcinoma.
Secretory adenocarcinoma.
Papillary or villoglandular.
Adenocarcinoma with squamous differentiation.
Adenoacanthoma.
Adenosquamous.
Uterine papillary serous (<10%).
Mucinous (1%).
Clear cell (4%).
Squamous cell (< 1%).
Mixed (10%).
Undifferentiated.
WHAT ARE THE RISK FACTORS OF UTERINE / ENDOMETRIAL CANCER?
Taking tamoxifen for breast cancer or taking estrogen alone (without progesterone) can affect the risk of developing endometrial cancer.
Endometrial cancer may develop in breast cancer patients who have been treated with tamoxifen. A patient taking this drug should have a pelvic examination every year and report any vaginal bleeding (other than menstrual bleeding) as soon as possible. Women taking estrogen (a hormone that can affect the growth of some cancers) alone have an increased risk of developing endometrial cancer. Taking estrogen in combination with progesterone (another hormone) does not increase a woman’s risk of this cancer.
HOW TO DETECT UTERINE / ENDOMETRIAL CANCER?
Possible signs of endometrial cancer include unusual vaginal discharge or pain in the pelvis.
Bleeding or discharge not related to menstruation (periods).
Difficult or painful urination.
Pain during sexual intercourse.
Pain in the pelvic area.
Tests that examine the endometrium are used to detect (find) and diagnose endometrial cancer.
One of the following procedures may be used to diagnose:
Endometrial biopsy: The removal of tissue from the endometrium (inner lining of the uterus) by inserting a thin, flexible tube through the cervix and into the uterus. The tube is used to gently scrape a small amount of tissue from the endometrium and then remove the tissue samples. A pathologist views the tissue under a microscope to look for cancer cells.
Dilatation and curettage: A surgical procedure to remove samples of tissue or the inner lining of the uterus. The cervix is dilated and a curette (spoon-shaped instrument) is inserted into the uterus to remove tissue. Tissue samples may be taken for biopsy. This procedure is also called a D&C.
Stage Information
A hysterectomy is required to determine the degree of myometrial invasion.
Stage I:carcinoma confined to the corpus uteri.
Stage IA: tumor limited to endometrium.
Stage IB: invasion to less than one half of the myometrium.
Stage IC: invasion to greater than one half of the myometrium.
Stage II: cancer involves the corpus and the cervix, but has not extended outside the uterus.
Stage IIA: endocervical glandular involvement only.
Stage IIB: cervical stromal invasion.
Stage III:cancer extends outside of the uterus but is confined to the true pelvis.
Stage IIIA: tumor invades serosa and/or adnexa and/or positive peritoneal cytology.
Stage IIIB: vaginal metastases.
Stage IIIC: metastases to pelvic and/or para-aortic lymph nodes.
Stage IV:cancer involves the bladder or bowel mucosa or has metastasized to distant sites.
Stage IVA: tumor invasion of bladder and/or bowel mucosa.
Stage IVB: distant metastases, including intra-abdominal and/or inguinal lymph nodes.
HOW TO TREAT UTERINE / ENDOMETRIAL CANCER?
Patients with endometrial cancer who have localized disease are usually curable by hysterectomy and bilateral salpingo-oophorectomy. Best results are obtained with either of 2 standard treatments: hysterectomy or hysterectomy and adjuvant radiation therapy (when deep invasion of the myometrial muscle [one half the depth] or grade 3 tumor with myometrial invasion is present). Results of a randomized trial on the use of adjuvant radiation therapy in patients with stage I disease did not show improved survival, but did show a significant increase in morbidity. Vaginal cuff brachytherapy, however, does not increase morbidity and reduces the risk of vaginal cuff recurrence without an effect on survival. Some patients have regional and distant metastases that, although occasionally responsive to standard hormone therapy, are rarely curable. For these patients, standard therapy is inadequate.
Progestational agents have been evaluated as adjuvant therapy in a randomized clinical trial of stage I disease and have been shown to be of no benefit. These studies, however, were not stratified according to level of progesterone receptor in the primary tumor. No trials of adjuvant progestins in more advanced disease are reported. Determination of progesterone receptors in the primary tumor is encouraged, and entry onto an appropriate adjuvant trial (if receptor levels are high) should be considered. If no trial is available, data from receptors on the primary tumor may help guide therapy for recurrent disease, should it occur.
Stage I Endometrial Cancer
Standard treatment options
If the tumor is well or moderately differentiated, involves the upper two thirds of the corpus, has negative peritoneal cytology, is without vascular space invasion, and has less than 50% myometrial invasion, a total abdominal hysterectomy and bilateral salpingo-oophorectomy should be done. Selected pelvic lymph nodes may be removed. If they are negative, no postoperative treatment is indicated. Postoperative treatment with a vaginal cylinder is advocated by some.
For all other cases and cell types, a periaortic and selective pelvic node sampling should be combined with the total abdominal hysterectomy and bilateral salpingo-oophorectomy if there are no medical or technical contraindications. One study found that node dissection per se did not significantly add to the overall morbidity from hysterectomy. While the irradiation will reduce the incidence of local and regional recurrence, improved survival has not been proven and toxic effects are worse.
If the pelvic nodes are positive and the periaortic nodes are negative, total pelvic irradiation, including the common iliac nodes, should be given. The incidence of bowel complications is approximately 4%, and it can be even higher if the radiation is given after pelvic lymphadenectomy. If the surgery is done using a retroperitoneal approach, the toxic effects are lessened. If the periaortic nodes are positive, the patient is a candidate for clinical trials that could include radiation and/or chemotherapy. Patients who have medical contraindications to surgery should be treated with radiation therapy alone, but inferior cure rates below those attained with surgery may occur.
Stage II Endometrial Cancer
Many combinations of preoperative intracavitary and external-beam radiation therapy with hysterectomy and bilateral salpingo-oophorectomy are used for treatment of stage II endometrial cancer, with careful biopsy of the para-aortic nodes at the time of surgery. When microscopic cervical stromal involvement is found, postoperative irradiation (external-beam and vaginal irradiation) should be used.
Stage IIA
Stage IIA (endocervical glandular involvement only) should be treated the same as stage I disease.
Stage IIB
Standard treatment options:
Hysterectomy, bilateral salpingo-oophorectomy, and node sampling followed by postoperative irradiation.
Preoperative intracavitary and external-beam radiation therapy followed by hysterectomy and bilateral salpingo-oophorectomy. (A biopsy of the para-aortic nodes should be done at the time of surgery.)
Radical hysterectomy and pelvic lymphadenectomy in selected cases.
Stage III Endometrial Cancer
Standard treatment options:
In general, these patients are treated with surgery and radiation therapy. These patients may be inoperable if the tumor extends to the pelvic wall, and in this case, they should be treated with radiation therapy. The usual approach is to use a combination of intracavitary and external-beam radiation therapy. Patients who are not candidates for either surgery or irradiation may be treated with progestational agents. Postoperative radiation therapy is used in patients who were thought to have had more localized disease (clinical stage I or II) but are found during hysterectomy to have positive lymph nodes or adnexa. Studies of patterns of failure have found a high rate of distant metastases in the upper abdominal and extra-abdominal sites. For this reason, patients with stage III disease may be candidates for innovative clinical trials.
Stage IV Endometrial Cancer
Standard treatment options
Treatment of stage IV endometrial cancer is dictated by the site of metastatic disease and symptoms related to disease sites. For bulky pelvic disease, radiation therapy consisting of a combination of intracavitary and external- beam irradiation is used. When distant metastases, especially pulmonary metastases, are present, hormonal therapy is indicated and useful.
The most common hormonal treatment has been progestational agents, which produce good antitumor responses in up to 15% to 30% of patients. These responses are associated with significant improvement in survival. Progesterone and estrogen hormone receptors have been identified in endometrial carcinoma tissues. Responses to hormones are correlated with the presence and level of hormone receptors and the degree of tumor differentiation. Standard progestational agents include hydroxyprogesterone (Delalutin), medroxyprogesterone (Provera), and megestrol (Megace).[1]
Recurrent Endometrial Cancer
For localized recurrences (pelvis and periaortic lymph nodes) or distant metastases in selected sites, irradiation may be an effective palliative therapy. In rare instances, pelvic irradiation may be curative in pure vaginal recurrence when no prior radiation has been used. Patients positive for estrogen and progesterone receptors respond best to progestin therapy. Among 115 patients with advanced endometrial cancer who were treated with progestins, 75% (42 of 56) of those with detectable progesterone receptors in their tumors before treatment responded, compared to only 7% without detectable progesterone receptors (4 of 59). A receptor-poor status may predict not only poor response to progestins, but also a better response to cytotoxic chemotherapy. There is evidence to suggest that tamoxifen (20 milligrams twice a day) will give a response rate of 20% in those who do not respond to standard progesterone therapy. Clinical trials are appropriate for patients whose disease recurs with distant metastases and who are unresponsive to hormonal therapy.[4] Doxorubicin is the most active anticancer agent employed, with useful but temporary responses obtained in up to one third of patients with metastatic disease. Paclitaxel also has significant activity.[5]
HOW TO DETECT THE PROGNOSIS OF UTERINE / ENDOMETRIAL CANCER?
Certain factors affect prognosis (chance of recovery) and treatment options,as the following:
The stage of the cancer (whether it is in the endometrium only, involves the whole uterus, or has spread to other places in the body).
How the cancer cells look under a microscope.
Whether the cancer cells are affected by progesterone.
Endometrial cancer is highly curable.
Endometrial cancer is a disease in which malignant (cancer) cells form in the tissues of the endometrium.
The endometrium is the lining of the uterus. The uterus is a hollow, muscular organ in a woman’s pelvis. The uterus is where a fetus grows. In most nonpregnant women, the uterus is about 3 inches long.
Cancer of the endometrium is different from cancer of the muscle of the uterus, which is called sarcoma of the uterus. Cancer of the endometrium is the most common gynecologic malignancy and accounts for 6% of all cancers in women. It is a highly curable tumor.
Cellular Classification
The most common endometrial cancer cell type is endometrioid adenocarcinoma, which is composed of malignant glandular epithelial elements; an admixture of squamous metaplasia is not uncommon. Adenosquamous tumors contain malignant elements of both glandular and squamous epithelium; clear cell and papillary serous carcinoma of the endometrium are tumors that are histologically similar to those noted in the ovary and the fallopian tube, and the prognosis is worse for these tumors. Mucinous, squamous, and undifferentiated tumors are rarely encountered. Frequency of endometrial cancer cell types is as follows:
Endometrioid (75%-80%)
Ciliated adenocarcinoma.
Secretory adenocarcinoma.
Papillary or villoglandular.
Adenocarcinoma with squamous differentiation.
Adenoacanthoma.
Adenosquamous.
Uterine papillary serous (<10%).
Mucinous (1%).
Clear cell (4%).
Squamous cell (< 1%).
Mixed (10%).
Undifferentiated.
WHAT ARE THE RISK FACTORS OF UTERINE / ENDOMETRIAL CANCER?
Taking tamoxifen for breast cancer or taking estrogen alone (without progesterone) can affect the risk of developing endometrial cancer.
Endometrial cancer may develop in breast cancer patients who have been treated with tamoxifen. A patient taking this drug should have a pelvic examination every year and report any vaginal bleeding (other than menstrual bleeding) as soon as possible. Women taking estrogen (a hormone that can affect the growth of some cancers) alone have an increased risk of developing endometrial cancer. Taking estrogen in combination with progesterone (another hormone) does not increase a woman’s risk of this cancer.
HOW TO DETECT UTERINE / ENDOMETRIAL CANCER?
Possible signs of endometrial cancer include unusual vaginal discharge or pain in the pelvis.
Bleeding or discharge not related to menstruation (periods).
Difficult or painful urination.
Pain during sexual intercourse.
Pain in the pelvic area.
Tests that examine the endometrium are used to detect (find) and diagnose endometrial cancer.
One of the following procedures may be used to diagnose:
Endometrial biopsy: The removal of tissue from the endometrium (inner lining of the uterus) by inserting a thin, flexible tube through the cervix and into the uterus. The tube is used to gently scrape a small amount of tissue from the endometrium and then remove the tissue samples. A pathologist views the tissue under a microscope to look for cancer cells.
Dilatation and curettage: A surgical procedure to remove samples of tissue or the inner lining of the uterus. The cervix is dilated and a curette (spoon-shaped instrument) is inserted into the uterus to remove tissue. Tissue samples may be taken for biopsy. This procedure is also called a D&C.
Stage Information
A hysterectomy is required to determine the degree of myometrial invasion.
Stage I:carcinoma confined to the corpus uteri.
Stage IA: tumor limited to endometrium.
Stage IB: invasion to less than one half of the myometrium.
Stage IC: invasion to greater than one half of the myometrium.
Stage II: cancer involves the corpus and the cervix, but has not extended outside the uterus.
Stage IIA: endocervical glandular involvement only.
Stage IIB: cervical stromal invasion.
Stage III:cancer extends outside of the uterus but is confined to the true pelvis.
Stage IIIA: tumor invades serosa and/or adnexa and/or positive peritoneal cytology.
Stage IIIB: vaginal metastases.
Stage IIIC: metastases to pelvic and/or para-aortic lymph nodes.
Stage IV:cancer involves the bladder or bowel mucosa or has metastasized to distant sites.
Stage IVA: tumor invasion of bladder and/or bowel mucosa.
Stage IVB: distant metastases, including intra-abdominal and/or inguinal lymph nodes.
HOW TO TREAT UTERINE / ENDOMETRIAL CANCER?
Patients with endometrial cancer who have localized disease are usually curable by hysterectomy and bilateral salpingo-oophorectomy. Best results are obtained with either of 2 standard treatments: hysterectomy or hysterectomy and adjuvant radiation therapy (when deep invasion of the myometrial muscle [one half the depth] or grade 3 tumor with myometrial invasion is present). Results of a randomized trial on the use of adjuvant radiation therapy in patients with stage I disease did not show improved survival, but did show a significant increase in morbidity. Vaginal cuff brachytherapy, however, does not increase morbidity and reduces the risk of vaginal cuff recurrence without an effect on survival. Some patients have regional and distant metastases that, although occasionally responsive to standard hormone therapy, are rarely curable. For these patients, standard therapy is inadequate.
Progestational agents have been evaluated as adjuvant therapy in a randomized clinical trial of stage I disease and have been shown to be of no benefit. These studies, however, were not stratified according to level of progesterone receptor in the primary tumor. No trials of adjuvant progestins in more advanced disease are reported. Determination of progesterone receptors in the primary tumor is encouraged, and entry onto an appropriate adjuvant trial (if receptor levels are high) should be considered. If no trial is available, data from receptors on the primary tumor may help guide therapy for recurrent disease, should it occur.
Stage I Endometrial Cancer
Standard treatment options
If the tumor is well or moderately differentiated, involves the upper two thirds of the corpus, has negative peritoneal cytology, is without vascular space invasion, and has less than 50% myometrial invasion, a total abdominal hysterectomy and bilateral salpingo-oophorectomy should be done. Selected pelvic lymph nodes may be removed. If they are negative, no postoperative treatment is indicated. Postoperative treatment with a vaginal cylinder is advocated by some.
For all other cases and cell types, a periaortic and selective pelvic node sampling should be combined with the total abdominal hysterectomy and bilateral salpingo-oophorectomy if there are no medical or technical contraindications. One study found that node dissection per se did not significantly add to the overall morbidity from hysterectomy. While the irradiation will reduce the incidence of local and regional recurrence, improved survival has not been proven and toxic effects are worse.
If the pelvic nodes are positive and the periaortic nodes are negative, total pelvic irradiation, including the common iliac nodes, should be given. The incidence of bowel complications is approximately 4%, and it can be even higher if the radiation is given after pelvic lymphadenectomy. If the surgery is done using a retroperitoneal approach, the toxic effects are lessened. If the periaortic nodes are positive, the patient is a candidate for clinical trials that could include radiation and/or chemotherapy. Patients who have medical contraindications to surgery should be treated with radiation therapy alone, but inferior cure rates below those attained with surgery may occur.
Stage II Endometrial Cancer
Many combinations of preoperative intracavitary and external-beam radiation therapy with hysterectomy and bilateral salpingo-oophorectomy are used for treatment of stage II endometrial cancer, with careful biopsy of the para-aortic nodes at the time of surgery. When microscopic cervical stromal involvement is found, postoperative irradiation (external-beam and vaginal irradiation) should be used.
Stage IIA
Stage IIA (endocervical glandular involvement only) should be treated the same as stage I disease.
Stage IIB
Standard treatment options:
Hysterectomy, bilateral salpingo-oophorectomy, and node sampling followed by postoperative irradiation.
Preoperative intracavitary and external-beam radiation therapy followed by hysterectomy and bilateral salpingo-oophorectomy. (A biopsy of the para-aortic nodes should be done at the time of surgery.)
Radical hysterectomy and pelvic lymphadenectomy in selected cases.
Stage III Endometrial Cancer
Standard treatment options:
In general, these patients are treated with surgery and radiation therapy. These patients may be inoperable if the tumor extends to the pelvic wall, and in this case, they should be treated with radiation therapy. The usual approach is to use a combination of intracavitary and external-beam radiation therapy. Patients who are not candidates for either surgery or irradiation may be treated with progestational agents. Postoperative radiation therapy is used in patients who were thought to have had more localized disease (clinical stage I or II) but are found during hysterectomy to have positive lymph nodes or adnexa. Studies of patterns of failure have found a high rate of distant metastases in the upper abdominal and extra-abdominal sites. For this reason, patients with stage III disease may be candidates for innovative clinical trials.
Stage IV Endometrial Cancer
Standard treatment options
Treatment of stage IV endometrial cancer is dictated by the site of metastatic disease and symptoms related to disease sites. For bulky pelvic disease, radiation therapy consisting of a combination of intracavitary and external- beam irradiation is used. When distant metastases, especially pulmonary metastases, are present, hormonal therapy is indicated and useful.
The most common hormonal treatment has been progestational agents, which produce good antitumor responses in up to 15% to 30% of patients. These responses are associated with significant improvement in survival. Progesterone and estrogen hormone receptors have been identified in endometrial carcinoma tissues. Responses to hormones are correlated with the presence and level of hormone receptors and the degree of tumor differentiation. Standard progestational agents include hydroxyprogesterone (Delalutin), medroxyprogesterone (Provera), and megestrol (Megace).[1]
Recurrent Endometrial Cancer
For localized recurrences (pelvis and periaortic lymph nodes) or distant metastases in selected sites, irradiation may be an effective palliative therapy. In rare instances, pelvic irradiation may be curative in pure vaginal recurrence when no prior radiation has been used. Patients positive for estrogen and progesterone receptors respond best to progestin therapy. Among 115 patients with advanced endometrial cancer who were treated with progestins, 75% (42 of 56) of those with detectable progesterone receptors in their tumors before treatment responded, compared to only 7% without detectable progesterone receptors (4 of 59). A receptor-poor status may predict not only poor response to progestins, but also a better response to cytotoxic chemotherapy. There is evidence to suggest that tamoxifen (20 milligrams twice a day) will give a response rate of 20% in those who do not respond to standard progesterone therapy. Clinical trials are appropriate for patients whose disease recurs with distant metastases and who are unresponsive to hormonal therapy.[4] Doxorubicin is the most active anticancer agent employed, with useful but temporary responses obtained in up to one third of patients with metastatic disease. Paclitaxel also has significant activity.[5]
HOW TO DETECT THE PROGNOSIS OF UTERINE / ENDOMETRIAL CANCER?
Certain factors affect prognosis (chance of recovery) and treatment options,as the following:
The stage of the cancer (whether it is in the endometrium only, involves the whole uterus, or has spread to other places in the body).
How the cancer cells look under a microscope.
Whether the cancer cells are affected by progesterone.
Endometrial cancer is highly curable.
Thyroid Cancer
WHAT IS THYROID CANCER?
The thyroid gland is at the base of the throat. It has two lobes, one on the right side and one on the left. The thyroid gland makes important hormones that help the body function normally. Thyroid cancer is a disease in which cancer (malignant) cells are found in the tissues of the thyroid gland.
Carcinoma of the thyroid gland is an uncommon cancer but is the most common malignancy of the endocrine system. Differentiated tumors (papillary or follicular) are highly treatable and usually curable. Poorly-differentiated tumors (medullary or anaplastic) are much less common, are aggressive, metastasize early, and have a much poorer prognosis. Thyroid cancer affects women more often than men, and usually occurs in people between the ages of 25 and 65 years. The incidence of this malignancy has been increasing over the last decade. Thyroid cancer commonly presents as a cold nodule. The overall incidence of cancer in a cold nodule is 12% to 15%, but it is higher in people younger than 40 years and in people with calcifications present on preoperative ultrasonography.
There are four main types of thyroid cancer (based on how the cancer cells look under a microscope):
papillary and follicular
medullary
anaplastic
WHAT ARE THE RISK FACTORS OF THYROID CANCER?
Patients with a history of radiation administered in infancy and childhood for benign conditions of the head and neck, such as enlarged thymus, acne, or tonsillar or adenoidal enlargement, have an increased risk of cancer as well as other abnormalities of the thyroid gland. In this group of patients, malignancies of the thyroid gland first appear beginning as early as 5 years following radiation and may appear 20 or more years later.
Radiation exposure as a consequence of nuclear fall-out has also been associated with a high risk of thyroid cancer, especially in children.
Other risk factors for the development of thyroid cancer include a history of goiter, family history of thyroid disease, female gender, and Asian race.
The thyroid gland may occasionally be the site of other primary tumors, including sarcomas, lymphomas, epidermoid carcinomas, and teratoma, and may be the site of metastasis from other cancers, particularly of the lung, breast, and kidney.
WHAT IS STAGE OF THYROID CANCER?
TNM definitions
Primary tumor (T)
[Note: All categories may be subdivided into (a) solitary tumor or (b) multifocal tumor (the largest determines the classification).]
TX: Primary tumor cannot be assessed
T0: No evidence of primary tumor
T1: Tumor 2 cm or less in greatest dimension, limited to the thyroid
T2: Tumor more than 2 cm but not more than 4 cm in greatest dimension, limited to the thyroid
T3: Tumor more than 4 cm in greatest dimension limited to the thyroid or any tumor with minimal extrathyroid extension (e.g., extension to sternothyroid muscle or perithyroid soft tissues)
T4a: Tumor of any size extending beyond the thyroid capsule to invade subcutaneous soft tissues, larynx, trachea, esophagus, or recurrent laryngeal nerve
T4b: Tumor invades prevertebral fascia or encases carotid artery or mediastinal vessels
All anaplastic carcinomas are considered T4 tumors.
T4a: Intrathyroidal anaplastic carcinoma—surgically resectable
T4b: Extrathyroidal anaplastic carcinoma—surgically unresectable.
Regional lymph nodes (N)
Regional lymph nodes are the central compartment, lateral cervical, and upper mediastinal lymph nodes.
NX: Regional lymph nodes cannot be assessed
N0: No regional lymph node metastasis
N1: Regional lymph node metastasis
N1a: Metastasis to level VI (pretracheal, paratracheal, and prelaryngeal/Delphian lymph nodes)
N1b: Metastasis to unilateral or bilateral cervical or superior mediastinal lymph nodes
Distant metastases (M)
MX: Distant metastasis cannot be assessed
M0: No distant metastasis
M1: Distant metastasis
AJCC stage groupings
Separate stage groupings are recommended for papillary or follicular, medullary, and anaplastic (undifferentiated) carcinoma.
Papillary or follicular thyroid cancer
Younger than 45 years
Stage I
Any T, any N, M0
Stage II
Any T, any N, M1
Age 45 years and older
Stage I
T1, N0, M0
Stage II
T2, N0, M0
Stage III
T3, N0, M0
T1, N1a, M0
T2, N1a, M0
T3, N1a, M0
Stage IVA
T4a, N0, M0
T4a, N1a, M0
T1, N1b, M0
T2, N1b, M0
T3, N1b, M0
T4a, N1b, M0
Stage IVB
T4b, any N, M0
Stage IVC
Any T, any N, M1
Medullary thyroid cancer
Stage I
T1, N0, M0
Stage II
T2, N0, M0
Stage III
T3, N0, M0
T1, N1a, M0
T2, N1a, M0
T3, N1a, M0
Stage IVA
T4a, N0, M0
T4a, N1a, M0
T1, N1b, M0
T2, N1b, M0
T3, N1b, M0
T4a, N1b, M0
Stage IVB
T4b, any N, M0
Stage IVC
Any T, any N, M1
Anaplastic thyroid cancer
All anaplastic carcinomas are considered stage IV.
Stage IVA
T4a, any N, M0
Stage IVB
T4b, any N, M0
Stage IVC
Any T, any N, M1
Papillary and follicular thyroid cancer
Stage I papillary thyroid cancer
Stage I papillary carcinoma is localized to the thyroid gland. In as many as 50% of cases there are multifocal sites of papillary adenocarcinomas throughout the gland. Most papillary cancers have some follicular elements, and these may sometimes be more numerous than the papillary formations, but this does not change the prognosis. The 10-year survival rate is slightly better for patients younger than 40 years than for patients older than 40 years.
Stage II papillary thyroid cancer
Stage II papillary carcinoma is defined as either (1) tumor that has spread distantly in patients younger than 45 years or (2) tumor that is larger than 2 cm but not more than 4 cm and is limited to the thyroid gland in patients older than 45 years. In as many as 50% to 80% of cases there are multifocal sites of papillary adenocarcinomas throughout the gland. Most papillary cancers have some follicular elements, and these may sometimes be more numerous than the papillary formations, but this does not appear to change the prognosis.
Stage III papillary thyroid cancer
Stage III is papillary carcinoma in patients older than 45 years that is larger than 4 cm and is limited to the thyroid or with minimal extrathyroid extension, or positive lymph nodes limited to the pretracheal, paratracheal, or prelaryngeal/Delphian nodes. Papillary carcinoma that has invaded adjacent cervical tissue has a worse prognosis than tumors confined to the thyroid.
Stage IV papillary thyroid cancer
Stage IV is papillary carcinoma in patients older than 45 years with extension beyond the thyroid capsule to the soft tissues of the neck, cervical lymph node metastases, or distant metastases. The lungs and bone are the most frequent distant sites of spread, although such distant spread is rare in this type of thyroid cancer. Papillary carcinoma more frequently metastasizes to regional lymph nodes than to distant sites. The prognosis for patients with distant metastases is poor.
Stage I follicular thyroid cancer
Stage I follicular carcinoma is localized to the thyroid gland. Follicular thyroid carcinoma must be distinguished from follicular adenomas, which are characterized by their lack of invasion through the capsule into the surrounding thyroid tissue. While follicular cancer has a good prognosis, it is less favorable than that of papillary carcinoma. The 10-year survival is better for patients with follicular carcinoma without vascular invasion than for patients with vascular invasion.
Stage II follicular thyroid cancer
Stage II follicular carcinoma is defined as either tumor that has spread distantly in patients younger than 45 years, or tumor that is larger than 2 cm but not more than 4 cm and is limited to the thyroid gland in patients older than 45 years. The presence of lymph node metastases does not worsen the prognosis among patients younger than 45 years. Follicular thyroid carcinoma must be distinguished from follicular adenomas, which are characterized by their lack of invasion through the capsule into the surrounding thyroid tissue. While follicular cancer has a good prognosis, it is less favorable than that of papillary carcinoma; the 10-year survival is better for patients with follicular carcinoma without vascular invasion than for patients with vascular invasion.
Stage III follicular thyroid cancer
Stage III is follicular carcinoma in patients older than 45 years, larger than 4 cm and limited to the thyroid or with minimal extrathyroid extension, or positive lymph nodes limited to the pretracheal, paratracheal, or prelaryngeal/Delphian nodes. Follicular carcinoma invading cervical tissue has a worse prognosis than tumors confined to the thyroid gland. The presence of vascular invasion is an additional poor prognostic factor. Metastases to lymph nodes do not worsen the prognosis in patients younger than 45 years.
Stage IV follicular thyroid cancer
Stage IV is follicular carcinoma in patients older than 45 years with extension beyond the thyroid capsule to the soft tissues of the neck, cervical lymph node metastases, or distant metastases. The lungs and bone are the most frequent sites of spread. Follicular carcinomas more commonly have blood vessel invasion and tend to metastasize hematogenously to the lungs and to the bone rather than through the lymphatic system. The prognosis for patients with distant metastases is poor.
Medullary thyroid cancer
Stage 0 medullary thyroid cancer
Clinically occult disease detected by provocative biochemical screening.
Stage I medullary thyroid cancer
Tumor less than 2 cm.
Stage II medullary thyroid cancer
Tumor larger than 2 cm but not more than 4 cm.
Stage III medullary thyroid cancer
Tumor larger than 4 cm with minimal extrathyroid extension or any primary tumor less than 4 cm with metastases limited to the pretracheal, paratracheal, or prelaryngeal/Delphian lymph nodes.
Stage IV medullary thyroid cancer
Stage IV medullary thyroid cancer is divided into:
Stage IVA (potentially resectable with or without lymph node metastases [for T4a] but without distant metastases).
Stage IVB (locally unresectable with or without lymph node metastases but no distant metastases).
Stage IVC (distant metastases).
Medullary carcinoma usually presents as a hard mass, and is often accompanied by blood vessel invasion. Medullary thyroid cancer occurs in 2 forms, sporadic and familial. In the sporadic form the tumor is usually unilateral. In the familial form, the tumor is almost always bilateral. In addition, the familial form may be associated with benign or malignant tumors of other endocrine organs, commonly referred to as the multiple endocrine neoplasia syndromes (MEN 2A or MEN 2B).
Family members should be screened for calcitonin elevation to identify individuals who are at risk of developing familial medullary thyroid cancer. MEN 2A gene carrier status can be more accurately determined by analysis of mutations in the RET gene. Whereas modest elevation of calcitonin may lead to a false-positive diagnosis of medullary carcinoma, DNA testing for the RET mutation is the optimal approach in evaluating MEN 2A. All patients with medullary carcinoma of the thyroid (whether familial or sporadic) should be tested for RET mutations, and, if they are positive, family members should also be tested. Family members who are gene carriers should undergo prophylactic thyroidectomy at an early age.
Anaplastic thyroid cancer
There is no generally accepted staging system for anaplastic thyroid cancer. All patients are considered to have stage IV disease.
Undifferentiated (anaplastic) carcinomas are highly malignant cancers of the thyroid. They may be subclassified as small cell or large cell carcinomas. Both grow rapidly and extend to structures beyond the thyroid. Both small cell and large cell carcinomas present as hard, ill-defined masses, often with extension into the structures surrounding the thyroid. Small cell anaplastic thyroid carcinoma must be carefully distinguished from lymphoma. This tumor usually occurs in an older age group and is characterized by extensive local invasion and rapid progression. Five-year survival with this tumor is poor. Death is usually from uncontrolled local cancer in the neck, usually within months of diagnosis.
HOW TO TREAT THYROID CANCER?
Papillary and Follicular Thyroid Cancer
Stage I and II
Surgery is the therapy of choice for all primary lesions. Surgical options include total thyroidectomy or lobectomy. The choice of procedure is influenced mainly by the age of the patient and the size of the nodule. Survival results may be similar; the difference between them lies in the rates of surgical complications and local recurrences.
Total thyroidectomy: This procedure is advocated because of the high incidence of multicentric involvement of both lobes of the gland and the possibility of dedifferentiation of any residual tumor to the anaplastic cell type. The procedure is associated with a higher incidence of hypoparathyroidism, but this complication may be reduced when a small amount of tissue remains on the contralateral side. This approach facilitates follow-up thyroid scanning.
I131:A postoperative course of therapeutic (ablative) doses of I131 results in a decreased recurrence rate among high-risk patients with papillary and follicular carcinomas. It may be given in addition to exogenous thyroid hormone, but is not considered routine. Patients presenting with papillary thyroid microcarcinomas (tumors <10 mm) have an excellent prognosis when treated surgically, and additional therapy with I131 would not be expected to improve the prognosis.
Lobectomy: This procedure is associated with a lower incidence of complications, but approximately 5% to 10% of patients will have a recurrence in the thyroid following lobectomy. Patients younger than 45 years will have the longest follow-up period and the greatest opportunity for recurrence. Follicular thyroid cancer commonly metastasizes to lungs and bone; with a remnant lobe in place, use of I131 as ablative therapy is compromised. Abnormal regional lymph nodes should be biopsied at the time of surgery. Recognized nodal involvement should be removed at initial surgery but selective node removal can be performed and radical neck dissection is usually not required. This results in a decreased recurrence rate, but has not been shown to improve survival.
Following the surgical procedure, patients should receive postoperative treatment with exogenous thyroid hormone in doses sufficient to suppress thyroid-stimulating hormone (TSH); studies have shown a decreased incidence of recurrence when TSH is suppressed.
I131: Studies have shown that a postoperative course of therapeutic (ablative) doses of I131 results in a decreased recurrence rate among high-risk patients with papillary and follicular carcinomas. It may be given in addition to exogenous thyroid hormone, but is not considered routine. Patients presenting with papillary thyroid microcarcinomas (tumors <10 mm) have an excellent prognosis when treated surgically, and additional therapy with I131 would not be expected to improve the prognosis.
Stage III
Total thyroidectomy plus removal of involved lymph nodes or other sites of extrathyroid disease.
I131 ablation following total thyroidectomy if the tumor demonstrates uptake of this isotope.
External-beam irradiation if I131 uptake is minimal.
Stage IV
The most common sites of metastases are lymph nodes, lung, and bone. Treatment of lymph node metastases alone is often curative. Treatment of distant metastases is usually not curative but may produce significant palliation.
I131: Metastases that demonstrate uptake of this isotope may be ablated by therapeutic doses of I131.
External-beam irradiation for patients with localized lesions that are unresponsive to I131.
Resection of limited metastases, especially symptomatic metastases, should be considered when the tumor has no uptake of I131.
Thyroid-stimulating hormone suppression with thyroxine is also effective in many lesions not sensitive to I131.
Patients unresponsive to I131 should also be considered candidates for clinical trials testing new approaches to this disease.
Medullary Thyroid Cancer
Medullary thyroid cancer (MTC) comprises 3% to 4% of all thyroid cancers. These tumors usually present as a mass in the neck or thyroid, often associated with lymphadenopathy, or they may be diagnosed through screening family members. MTC can also be diagnosed by fine-needle aspiration biopsy. Cytology typically reveals hypercellular tumors with spindle-shaped cells and poor adhesion.
The overall survival of patients with MTC is 86% at 5 years and 65% at 10 years. Poor prognostic factors include advanced age, advanced stage, prior neck surgery, and associated-multiple endocrine neoplasia (MEN) 2B.
Family members should be screened for calcitonin elevation and/or for the RET proto-oncogene mutation to identify other individuals at risk for developing familial MTC. All patients with MTC (whether familial or sporadic) should be tested for RET mutations, and if they are positive, family members should also be tested. Whereas modest elevation of calcitonin may lead to a false-positive diagnosis of medullary carcinoma, DNA testing for the RET mutation is the optimal approach. Family members who are gene carriers should undergo prophylactic thyroidectomy at an early age.
Thyroidectomy: Patients with medullary thyroid cancer should be treated with a total thyroidectomy, unless there is evidence of distant metastasis. In patients with clinically palpable medullary carcinoma of the thyroid, the incidence of microscopically positive nodes is more than 75%; routine central and bilateral modified neck dissections have been recommended. When cancer is confined to the thyroid gland, the prognosis is excellent.
External radiation therapy: External radiation therapy has been used for palliation of locally-recurrent tumors, without evidence that it provides any survival advantage. Radioactive iodine has no place in the treatment of patients with MTC.
Palliative chemotherapy: Palliative chemotherapy has been reported to produce occasional responses in patients with metastatic disease. No single drug regimen can be considered standard. Some patients with distant metastases will experience prolonged survival, and can be managed expectantly until they become symptomatic.
Anaplastic Thyroid Cancer
Surgery: Tracheostomy is frequently necessary. If the disease is confined to the local area, which is rare, total thyroidectomy is warranted to reduce symptoms caused by the tumor mass.
Radiation therapy: External beam radiation therapy may be used in patients who are not surgical candidates or whose tumor cannot be surgically excised.
Chemotherapy: Anaplastic thyroid cancer is not responsive to I131 therapy; treatment with individual anticancer drugs has been reported to produce partial remissions in some patients. Approximately 30% of patients achieve a partial remission with doxorubicin. The combination of doxorubicin plus cisplatin appears to be more active than doxorubicin alone and has been reported to produce more complete responses.
The combination of chemotherapy plus irradiation in patients following complete resection may provide prolonged survival, but has not been compared to any one modality alone.[5] Clinical trials evaluating new treatment approaches for this disease should also be considered.
Recurrent Thyroid Cancer
Patients treated for differentiated thyroid cancer should be followed carefully with physical examinations, serum quantitative thyroglobulin levels, and radiologic studies based on individual risk for recurrent disease. Approximately 10% to 30% of patients thought to be disease-free after initial treatment will develop recurrence and/or metastases. Of patients who recur, approximately 80% recur with disease in the neck alone and 20% with distant metastases. The most common site of distant metastasis is the lung.
The prognosis for patients with clinically detectable recurrences is generally poor, regardless of cell type. However, those patients who recur with local or regional tumor detected only by I131 scan have a better prognosis. The selection of further treatment depends on many factors, including cell type, uptake of I131, prior treatment, site of recurrence, and individual patient considerations. Surgery with or without I131 ablation can be useful in controlling local recurrences, regional node metastases, or, occasionally, metastases at other localized sites. Approximately half of the patients operated on for recurrent tumors can be rendered free of disease with a second operation. Local and regional recurrences detected by I131 scan and not clinically apparent can be treated with I131 ablation and have an excellent prognosis.
Up to 25% of recurrences and metastases from well-differentiated thyroid cancer may not show I131 uptake. For these patients, other imaging techniques shown to be of value include imaging with thallium-201, magnetic resonance imaging, and pentavalent dimercaptosuccinic acid. When recurrent disease does not concentrate I131, external-beam or intraoperative radiation therapy can be useful in controlling symptoms related to local tumor recurrences. Systemic chemotherapy can be considered. Chemotherapy has been reported to produce occasional objective responses, usually of short duration.
WHAT ARE THE PROGNOSTIC FACTORS OF THYROID CANCER?
Age appears to be the single most important prognostic factor. The prognosis for differentiated carcinoma is better for patients younger than 40 years without extracapsular extension or vascular invasion. Female gender, multifocality, and regional node involvement are favorable prognostic factors. Adverse factors included age older than 45 years, follicular histology, primary tumor larger than 4 cm (T2-3), extrathyroid extension (T4), and distant metastases.
Other studies, however, have shown that regional lymph node involvement had no effect or even an adverse effect on survival.
Diffuse, intense immunostaining for vascular endothelial growth factor in patients with papillary cancer has been associated with a high rate of local recurrence and distant metastases.
An elevated serum thyroglobulin level correlates strongly with recurrent tumor when found in patients with differentiated thyroid cancer during postoperative evaluations. Serum thyroglobulin levels are most sensitive when patients are hypothyroid and have elevated serum thyroid-stimulating hormone levels.
Expression of the tumor suppressor gene p53 has also been associated with an adverse prognosis for patients with thyroid cancer.
Patients considered to be low risk by the age, metastases, extent, and size (AMES) risk criteria include women younger than 50 years and men younger than 40 years without evidence of distant metastases. Also included in the low-risk group are older patients with primary tumors less than 5 cm and papillary cancer without evidence of gross extrathyroid invasion or follicular cancer without either major capsular invasion or blood vessel invasion.
The thyroid gland is at the base of the throat. It has two lobes, one on the right side and one on the left. The thyroid gland makes important hormones that help the body function normally. Thyroid cancer is a disease in which cancer (malignant) cells are found in the tissues of the thyroid gland.
Carcinoma of the thyroid gland is an uncommon cancer but is the most common malignancy of the endocrine system. Differentiated tumors (papillary or follicular) are highly treatable and usually curable. Poorly-differentiated tumors (medullary or anaplastic) are much less common, are aggressive, metastasize early, and have a much poorer prognosis. Thyroid cancer affects women more often than men, and usually occurs in people between the ages of 25 and 65 years. The incidence of this malignancy has been increasing over the last decade. Thyroid cancer commonly presents as a cold nodule. The overall incidence of cancer in a cold nodule is 12% to 15%, but it is higher in people younger than 40 years and in people with calcifications present on preoperative ultrasonography.
There are four main types of thyroid cancer (based on how the cancer cells look under a microscope):
papillary and follicular
medullary
anaplastic
WHAT ARE THE RISK FACTORS OF THYROID CANCER?
Patients with a history of radiation administered in infancy and childhood for benign conditions of the head and neck, such as enlarged thymus, acne, or tonsillar or adenoidal enlargement, have an increased risk of cancer as well as other abnormalities of the thyroid gland. In this group of patients, malignancies of the thyroid gland first appear beginning as early as 5 years following radiation and may appear 20 or more years later.
Radiation exposure as a consequence of nuclear fall-out has also been associated with a high risk of thyroid cancer, especially in children.
Other risk factors for the development of thyroid cancer include a history of goiter, family history of thyroid disease, female gender, and Asian race.
The thyroid gland may occasionally be the site of other primary tumors, including sarcomas, lymphomas, epidermoid carcinomas, and teratoma, and may be the site of metastasis from other cancers, particularly of the lung, breast, and kidney.
WHAT IS STAGE OF THYROID CANCER?
TNM definitions
Primary tumor (T)
[Note: All categories may be subdivided into (a) solitary tumor or (b) multifocal tumor (the largest determines the classification).]
TX: Primary tumor cannot be assessed
T0: No evidence of primary tumor
T1: Tumor 2 cm or less in greatest dimension, limited to the thyroid
T2: Tumor more than 2 cm but not more than 4 cm in greatest dimension, limited to the thyroid
T3: Tumor more than 4 cm in greatest dimension limited to the thyroid or any tumor with minimal extrathyroid extension (e.g., extension to sternothyroid muscle or perithyroid soft tissues)
T4a: Tumor of any size extending beyond the thyroid capsule to invade subcutaneous soft tissues, larynx, trachea, esophagus, or recurrent laryngeal nerve
T4b: Tumor invades prevertebral fascia or encases carotid artery or mediastinal vessels
All anaplastic carcinomas are considered T4 tumors.
T4a: Intrathyroidal anaplastic carcinoma—surgically resectable
T4b: Extrathyroidal anaplastic carcinoma—surgically unresectable.
Regional lymph nodes (N)
Regional lymph nodes are the central compartment, lateral cervical, and upper mediastinal lymph nodes.
NX: Regional lymph nodes cannot be assessed
N0: No regional lymph node metastasis
N1: Regional lymph node metastasis
N1a: Metastasis to level VI (pretracheal, paratracheal, and prelaryngeal/Delphian lymph nodes)
N1b: Metastasis to unilateral or bilateral cervical or superior mediastinal lymph nodes
Distant metastases (M)
MX: Distant metastasis cannot be assessed
M0: No distant metastasis
M1: Distant metastasis
AJCC stage groupings
Separate stage groupings are recommended for papillary or follicular, medullary, and anaplastic (undifferentiated) carcinoma.
Papillary or follicular thyroid cancer
Younger than 45 years
Stage I
Any T, any N, M0
Stage II
Any T, any N, M1
Age 45 years and older
Stage I
T1, N0, M0
Stage II
T2, N0, M0
Stage III
T3, N0, M0
T1, N1a, M0
T2, N1a, M0
T3, N1a, M0
Stage IVA
T4a, N0, M0
T4a, N1a, M0
T1, N1b, M0
T2, N1b, M0
T3, N1b, M0
T4a, N1b, M0
Stage IVB
T4b, any N, M0
Stage IVC
Any T, any N, M1
Medullary thyroid cancer
Stage I
T1, N0, M0
Stage II
T2, N0, M0
Stage III
T3, N0, M0
T1, N1a, M0
T2, N1a, M0
T3, N1a, M0
Stage IVA
T4a, N0, M0
T4a, N1a, M0
T1, N1b, M0
T2, N1b, M0
T3, N1b, M0
T4a, N1b, M0
Stage IVB
T4b, any N, M0
Stage IVC
Any T, any N, M1
Anaplastic thyroid cancer
All anaplastic carcinomas are considered stage IV.
Stage IVA
T4a, any N, M0
Stage IVB
T4b, any N, M0
Stage IVC
Any T, any N, M1
Papillary and follicular thyroid cancer
Stage I papillary thyroid cancer
Stage I papillary carcinoma is localized to the thyroid gland. In as many as 50% of cases there are multifocal sites of papillary adenocarcinomas throughout the gland. Most papillary cancers have some follicular elements, and these may sometimes be more numerous than the papillary formations, but this does not change the prognosis. The 10-year survival rate is slightly better for patients younger than 40 years than for patients older than 40 years.
Stage II papillary thyroid cancer
Stage II papillary carcinoma is defined as either (1) tumor that has spread distantly in patients younger than 45 years or (2) tumor that is larger than 2 cm but not more than 4 cm and is limited to the thyroid gland in patients older than 45 years. In as many as 50% to 80% of cases there are multifocal sites of papillary adenocarcinomas throughout the gland. Most papillary cancers have some follicular elements, and these may sometimes be more numerous than the papillary formations, but this does not appear to change the prognosis.
Stage III papillary thyroid cancer
Stage III is papillary carcinoma in patients older than 45 years that is larger than 4 cm and is limited to the thyroid or with minimal extrathyroid extension, or positive lymph nodes limited to the pretracheal, paratracheal, or prelaryngeal/Delphian nodes. Papillary carcinoma that has invaded adjacent cervical tissue has a worse prognosis than tumors confined to the thyroid.
Stage IV papillary thyroid cancer
Stage IV is papillary carcinoma in patients older than 45 years with extension beyond the thyroid capsule to the soft tissues of the neck, cervical lymph node metastases, or distant metastases. The lungs and bone are the most frequent distant sites of spread, although such distant spread is rare in this type of thyroid cancer. Papillary carcinoma more frequently metastasizes to regional lymph nodes than to distant sites. The prognosis for patients with distant metastases is poor.
Stage I follicular thyroid cancer
Stage I follicular carcinoma is localized to the thyroid gland. Follicular thyroid carcinoma must be distinguished from follicular adenomas, which are characterized by their lack of invasion through the capsule into the surrounding thyroid tissue. While follicular cancer has a good prognosis, it is less favorable than that of papillary carcinoma. The 10-year survival is better for patients with follicular carcinoma without vascular invasion than for patients with vascular invasion.
Stage II follicular thyroid cancer
Stage II follicular carcinoma is defined as either tumor that has spread distantly in patients younger than 45 years, or tumor that is larger than 2 cm but not more than 4 cm and is limited to the thyroid gland in patients older than 45 years. The presence of lymph node metastases does not worsen the prognosis among patients younger than 45 years. Follicular thyroid carcinoma must be distinguished from follicular adenomas, which are characterized by their lack of invasion through the capsule into the surrounding thyroid tissue. While follicular cancer has a good prognosis, it is less favorable than that of papillary carcinoma; the 10-year survival is better for patients with follicular carcinoma without vascular invasion than for patients with vascular invasion.
Stage III follicular thyroid cancer
Stage III is follicular carcinoma in patients older than 45 years, larger than 4 cm and limited to the thyroid or with minimal extrathyroid extension, or positive lymph nodes limited to the pretracheal, paratracheal, or prelaryngeal/Delphian nodes. Follicular carcinoma invading cervical tissue has a worse prognosis than tumors confined to the thyroid gland. The presence of vascular invasion is an additional poor prognostic factor. Metastases to lymph nodes do not worsen the prognosis in patients younger than 45 years.
Stage IV follicular thyroid cancer
Stage IV is follicular carcinoma in patients older than 45 years with extension beyond the thyroid capsule to the soft tissues of the neck, cervical lymph node metastases, or distant metastases. The lungs and bone are the most frequent sites of spread. Follicular carcinomas more commonly have blood vessel invasion and tend to metastasize hematogenously to the lungs and to the bone rather than through the lymphatic system. The prognosis for patients with distant metastases is poor.
Medullary thyroid cancer
Stage 0 medullary thyroid cancer
Clinically occult disease detected by provocative biochemical screening.
Stage I medullary thyroid cancer
Tumor less than 2 cm.
Stage II medullary thyroid cancer
Tumor larger than 2 cm but not more than 4 cm.
Stage III medullary thyroid cancer
Tumor larger than 4 cm with minimal extrathyroid extension or any primary tumor less than 4 cm with metastases limited to the pretracheal, paratracheal, or prelaryngeal/Delphian lymph nodes.
Stage IV medullary thyroid cancer
Stage IV medullary thyroid cancer is divided into:
Stage IVA (potentially resectable with or without lymph node metastases [for T4a] but without distant metastases).
Stage IVB (locally unresectable with or without lymph node metastases but no distant metastases).
Stage IVC (distant metastases).
Medullary carcinoma usually presents as a hard mass, and is often accompanied by blood vessel invasion. Medullary thyroid cancer occurs in 2 forms, sporadic and familial. In the sporadic form the tumor is usually unilateral. In the familial form, the tumor is almost always bilateral. In addition, the familial form may be associated with benign or malignant tumors of other endocrine organs, commonly referred to as the multiple endocrine neoplasia syndromes (MEN 2A or MEN 2B).
Family members should be screened for calcitonin elevation to identify individuals who are at risk of developing familial medullary thyroid cancer. MEN 2A gene carrier status can be more accurately determined by analysis of mutations in the RET gene. Whereas modest elevation of calcitonin may lead to a false-positive diagnosis of medullary carcinoma, DNA testing for the RET mutation is the optimal approach in evaluating MEN 2A. All patients with medullary carcinoma of the thyroid (whether familial or sporadic) should be tested for RET mutations, and, if they are positive, family members should also be tested. Family members who are gene carriers should undergo prophylactic thyroidectomy at an early age.
Anaplastic thyroid cancer
There is no generally accepted staging system for anaplastic thyroid cancer. All patients are considered to have stage IV disease.
Undifferentiated (anaplastic) carcinomas are highly malignant cancers of the thyroid. They may be subclassified as small cell or large cell carcinomas. Both grow rapidly and extend to structures beyond the thyroid. Both small cell and large cell carcinomas present as hard, ill-defined masses, often with extension into the structures surrounding the thyroid. Small cell anaplastic thyroid carcinoma must be carefully distinguished from lymphoma. This tumor usually occurs in an older age group and is characterized by extensive local invasion and rapid progression. Five-year survival with this tumor is poor. Death is usually from uncontrolled local cancer in the neck, usually within months of diagnosis.
HOW TO TREAT THYROID CANCER?
Papillary and Follicular Thyroid Cancer
Stage I and II
Surgery is the therapy of choice for all primary lesions. Surgical options include total thyroidectomy or lobectomy. The choice of procedure is influenced mainly by the age of the patient and the size of the nodule. Survival results may be similar; the difference between them lies in the rates of surgical complications and local recurrences.
Total thyroidectomy: This procedure is advocated because of the high incidence of multicentric involvement of both lobes of the gland and the possibility of dedifferentiation of any residual tumor to the anaplastic cell type. The procedure is associated with a higher incidence of hypoparathyroidism, but this complication may be reduced when a small amount of tissue remains on the contralateral side. This approach facilitates follow-up thyroid scanning.
I131:A postoperative course of therapeutic (ablative) doses of I131 results in a decreased recurrence rate among high-risk patients with papillary and follicular carcinomas. It may be given in addition to exogenous thyroid hormone, but is not considered routine. Patients presenting with papillary thyroid microcarcinomas (tumors <10 mm) have an excellent prognosis when treated surgically, and additional therapy with I131 would not be expected to improve the prognosis.
Lobectomy: This procedure is associated with a lower incidence of complications, but approximately 5% to 10% of patients will have a recurrence in the thyroid following lobectomy. Patients younger than 45 years will have the longest follow-up period and the greatest opportunity for recurrence. Follicular thyroid cancer commonly metastasizes to lungs and bone; with a remnant lobe in place, use of I131 as ablative therapy is compromised. Abnormal regional lymph nodes should be biopsied at the time of surgery. Recognized nodal involvement should be removed at initial surgery but selective node removal can be performed and radical neck dissection is usually not required. This results in a decreased recurrence rate, but has not been shown to improve survival.
Following the surgical procedure, patients should receive postoperative treatment with exogenous thyroid hormone in doses sufficient to suppress thyroid-stimulating hormone (TSH); studies have shown a decreased incidence of recurrence when TSH is suppressed.
I131: Studies have shown that a postoperative course of therapeutic (ablative) doses of I131 results in a decreased recurrence rate among high-risk patients with papillary and follicular carcinomas. It may be given in addition to exogenous thyroid hormone, but is not considered routine. Patients presenting with papillary thyroid microcarcinomas (tumors <10 mm) have an excellent prognosis when treated surgically, and additional therapy with I131 would not be expected to improve the prognosis.
Stage III
Total thyroidectomy plus removal of involved lymph nodes or other sites of extrathyroid disease.
I131 ablation following total thyroidectomy if the tumor demonstrates uptake of this isotope.
External-beam irradiation if I131 uptake is minimal.
Stage IV
The most common sites of metastases are lymph nodes, lung, and bone. Treatment of lymph node metastases alone is often curative. Treatment of distant metastases is usually not curative but may produce significant palliation.
I131: Metastases that demonstrate uptake of this isotope may be ablated by therapeutic doses of I131.
External-beam irradiation for patients with localized lesions that are unresponsive to I131.
Resection of limited metastases, especially symptomatic metastases, should be considered when the tumor has no uptake of I131.
Thyroid-stimulating hormone suppression with thyroxine is also effective in many lesions not sensitive to I131.
Patients unresponsive to I131 should also be considered candidates for clinical trials testing new approaches to this disease.
Medullary Thyroid Cancer
Medullary thyroid cancer (MTC) comprises 3% to 4% of all thyroid cancers. These tumors usually present as a mass in the neck or thyroid, often associated with lymphadenopathy, or they may be diagnosed through screening family members. MTC can also be diagnosed by fine-needle aspiration biopsy. Cytology typically reveals hypercellular tumors with spindle-shaped cells and poor adhesion.
The overall survival of patients with MTC is 86% at 5 years and 65% at 10 years. Poor prognostic factors include advanced age, advanced stage, prior neck surgery, and associated-multiple endocrine neoplasia (MEN) 2B.
Family members should be screened for calcitonin elevation and/or for the RET proto-oncogene mutation to identify other individuals at risk for developing familial MTC. All patients with MTC (whether familial or sporadic) should be tested for RET mutations, and if they are positive, family members should also be tested. Whereas modest elevation of calcitonin may lead to a false-positive diagnosis of medullary carcinoma, DNA testing for the RET mutation is the optimal approach. Family members who are gene carriers should undergo prophylactic thyroidectomy at an early age.
Thyroidectomy: Patients with medullary thyroid cancer should be treated with a total thyroidectomy, unless there is evidence of distant metastasis. In patients with clinically palpable medullary carcinoma of the thyroid, the incidence of microscopically positive nodes is more than 75%; routine central and bilateral modified neck dissections have been recommended. When cancer is confined to the thyroid gland, the prognosis is excellent.
External radiation therapy: External radiation therapy has been used for palliation of locally-recurrent tumors, without evidence that it provides any survival advantage. Radioactive iodine has no place in the treatment of patients with MTC.
Palliative chemotherapy: Palliative chemotherapy has been reported to produce occasional responses in patients with metastatic disease. No single drug regimen can be considered standard. Some patients with distant metastases will experience prolonged survival, and can be managed expectantly until they become symptomatic.
Anaplastic Thyroid Cancer
Surgery: Tracheostomy is frequently necessary. If the disease is confined to the local area, which is rare, total thyroidectomy is warranted to reduce symptoms caused by the tumor mass.
Radiation therapy: External beam radiation therapy may be used in patients who are not surgical candidates or whose tumor cannot be surgically excised.
Chemotherapy: Anaplastic thyroid cancer is not responsive to I131 therapy; treatment with individual anticancer drugs has been reported to produce partial remissions in some patients. Approximately 30% of patients achieve a partial remission with doxorubicin. The combination of doxorubicin plus cisplatin appears to be more active than doxorubicin alone and has been reported to produce more complete responses.
The combination of chemotherapy plus irradiation in patients following complete resection may provide prolonged survival, but has not been compared to any one modality alone.[5] Clinical trials evaluating new treatment approaches for this disease should also be considered.
Recurrent Thyroid Cancer
Patients treated for differentiated thyroid cancer should be followed carefully with physical examinations, serum quantitative thyroglobulin levels, and radiologic studies based on individual risk for recurrent disease. Approximately 10% to 30% of patients thought to be disease-free after initial treatment will develop recurrence and/or metastases. Of patients who recur, approximately 80% recur with disease in the neck alone and 20% with distant metastases. The most common site of distant metastasis is the lung.
The prognosis for patients with clinically detectable recurrences is generally poor, regardless of cell type. However, those patients who recur with local or regional tumor detected only by I131 scan have a better prognosis. The selection of further treatment depends on many factors, including cell type, uptake of I131, prior treatment, site of recurrence, and individual patient considerations. Surgery with or without I131 ablation can be useful in controlling local recurrences, regional node metastases, or, occasionally, metastases at other localized sites. Approximately half of the patients operated on for recurrent tumors can be rendered free of disease with a second operation. Local and regional recurrences detected by I131 scan and not clinically apparent can be treated with I131 ablation and have an excellent prognosis.
Up to 25% of recurrences and metastases from well-differentiated thyroid cancer may not show I131 uptake. For these patients, other imaging techniques shown to be of value include imaging with thallium-201, magnetic resonance imaging, and pentavalent dimercaptosuccinic acid. When recurrent disease does not concentrate I131, external-beam or intraoperative radiation therapy can be useful in controlling symptoms related to local tumor recurrences. Systemic chemotherapy can be considered. Chemotherapy has been reported to produce occasional objective responses, usually of short duration.
WHAT ARE THE PROGNOSTIC FACTORS OF THYROID CANCER?
Age appears to be the single most important prognostic factor. The prognosis for differentiated carcinoma is better for patients younger than 40 years without extracapsular extension or vascular invasion. Female gender, multifocality, and regional node involvement are favorable prognostic factors. Adverse factors included age older than 45 years, follicular histology, primary tumor larger than 4 cm (T2-3), extrathyroid extension (T4), and distant metastases.
Other studies, however, have shown that regional lymph node involvement had no effect or even an adverse effect on survival.
Diffuse, intense immunostaining for vascular endothelial growth factor in patients with papillary cancer has been associated with a high rate of local recurrence and distant metastases.
An elevated serum thyroglobulin level correlates strongly with recurrent tumor when found in patients with differentiated thyroid cancer during postoperative evaluations. Serum thyroglobulin levels are most sensitive when patients are hypothyroid and have elevated serum thyroid-stimulating hormone levels.
Expression of the tumor suppressor gene p53 has also been associated with an adverse prognosis for patients with thyroid cancer.
Patients considered to be low risk by the age, metastases, extent, and size (AMES) risk criteria include women younger than 50 years and men younger than 40 years without evidence of distant metastases. Also included in the low-risk group are older patients with primary tumors less than 5 cm and papillary cancer without evidence of gross extrathyroid invasion or follicular cancer without either major capsular invasion or blood vessel invasion.
Thymoma and Thymic Carcinoma
WHAT ARE THYMOMA AND THYMIC CARCINOMA?
The thymus is a small organ that lies under the breastbone. It makes white blood cells called lymphocytes that travel through the body and fight infection.
Thymoma and thymic carcinoma are diseases in which cancer (malignant) cells are found in the tissues of the thymus. Thymomas are epithelial tumors of the thymus, which may or may not be extensively infiltrated by nonneoplastic lymphocytes. The term thymoma is customarily used to describe neoplasms that show no overt atypia of the epithelial component. A thymic epithelial tumor that exhibits clear-cut cytologic atypia and histologic features no longer specific to the thymus is known as a thymic carcinoma (also known as type C thymoma).
Invasive thymomas and thymic carcinomas are relatively rare tumors, together representing about 0.2% to 1.5% of all malignancies. Thymic carcinomas are rare and have been reported to account for only 0.06% of all thymic neoplasms. In general, thymomas are indolent tumors with a tendency toward local recurrence rather than metastasis. Thymic carcinomas, however, are typically invasive, with a high risk of relapse and death.
Most patients with thymoma or thymic carcinoma are aged 40 through 60 years. The etiology of these tumors is not known. In about half of cases, thymomas/thymic carcinomas are detected by chance with plain-film chest radiography. Ninety percent occur in the anterior mediastinum.
HOW TO DETECT THYMOMA AND THYMIC CARCINOMA?
Symptoms
The following symptoms suggest thymoma or thymic carcinoma:
A cough that won’t go away.
Pain in the chest.
Weakness in the muscles.
Approximately 30% of patients with thymoma/thymic carcinoma are asymptomatic at the time of diagnosis. In other cases, the presenting clinical signs of these tumors may include coughing, chest pain, and signs of upper airway congestion.
Paraneoplastic autoimmune syndromes associated with thymoma include myasthenia gravis, polymyositis, lupus erythematosus, rheumatoid arthritis, thyroiditis, and Sj?gren’s syndrome, among others. Autoimmune pure red cell aplasia and hypogammaglobulinemia each affect approximately 5% of patients with thymoma.
Thymoma-associated autoimmune disease involves an alteration in circulating T-cell subsets. In addition, B-cell lymphopenia has been observed in thymoma-related immunodeficiency, with hypogammaglobulinemia (Good syndrome) and opportunistic infection. In contrast to thymoma, the association of thymic carcinoma and autoimmune diseases is rare.
Approximately 47% of thymoma cases (excluding thymic carcinoma) were found to be associated with myasthenia gravis.
Stage
Histologic classification of thymoma is not sufficient to distinguish biologically benign thymomas from malignant thymomas. The degree of invasion or tumor stage is generally thought to be a more important indicator of overall survival.
Evaluating the invasiveness of a thymoma involves the use of staging criteria that indicate the presence and degree of contiguous invasion, the presence of implants, and lymph node or distant metastases regardless of histologic type. The following staging system is commonly employed and is shown below.
Thymoma Staging System
Stage
Description
I
Macroscopically, completely encapsulated; microscopically, no capsular invasion
II
Macroscopic invasion into surrounding fatty tissue or mediastinal pleura; microscopic invasion into capsule
III
Macroscopic invasion into neighboring organs (pericardium, lung, great vessels)
IVa
Pleural or pericardial dissemination
IVb
Lymphogenous or hematogenous metastases
For the purposes of treatment, these stages are grouped as either noninvasive or invasive.
Noninvasive
In noninvasive (stage I) disease, the tumor is limited to the thymus gland and has not involved other tissues. All of the tumor cells remain within a fibrous capsule that surrounds the tumor.
Invasive
In locally invasive (stage II) disease, the tumor has broken through the capsule and invaded the fat or pleura. In extensively invasive (stages III and IVa) disease, the tumor has spread contiguously from the thymus gland to involve other organs in the chest. Spread to organs in the abdomen or metastatic embolic spread (stage IVb) is unusual at the time of presentation.
Computed tomography (CT) may be useful in the diagnosis and clinical staging of thymoma, especially for noninvasive tumors. It is usually accurate in predicting tumor size, location, and invasion into vessels, the pericardium, and the lung. It cannot predict, however, invasion or resectability with accuracy. Appearance of the tumor on CT may be related to the World Health Organization histologic type. The smooth contours and a round shape are most suggestive of type A thymomas, whereas irregular contours are most suggestive of thymic carcinomas. Calcification is suggestive of type B thymomas.
HOW TO TREAT THYMOMA AND THYMIC CARCINOMA?
Most thymomas are diagnosed and staged at the time of surgical intervention. Surgical resection is the preferred treatment of patients who can tolerate surgery and have a mediastinal mass that is suspected of being a thymoma. A total thymectomy with complete resection of all tumor can be achieved in nearly all stage I and stage II patients and in 27% to 44% of stage III patients. Postoperative radiation therapy is generally employed for stage II and stage III patients. Patients with stage IVa disease can only rarely be resected completely and are usually offered debulking surgery and postoperative radiation therapy, with or without chemotherapy.
Noninvasive Thymoma and Thymic Carcinoma
Standard treatment options
Surgical resection: Complete resection of a well-encapsulated, noninvasive thymoma is usually curative, with a risk of local recurrence of less than 2%. In patients with myasthenia gravis, operative mortality can be minimized with close attention to respiratory support when planning surgical treatment.
Radiation therapy is not indicated following complete resection of a well-encapsulated thymoma. Radiation therapy should be considered, however, in rare cases when a noninvasive thymoma is incompletely resected, and when the patient is a poor surgical risk.
Invasive Thymoma and Thymic Carcinoma
Operable
En bloc surgical resection if possible. In patients with myasthenia gravis, operative mortality can be minimized with close attention to respiratory support when planning surgical treatment.
Following surgical resection, radiation therapy is generally recommended whether or not the surgical resection has been complete, especially for stage III and stage IVa patients. Retrospective clinical studies show improved local control and survival with the addition of postoperative radiation therapy.
Inoperable (stages III and IV with vena caval obstruction, pleural involvement, pericardial implants, etc.)
Radiation therapy: In patients who have residual macroscopic tumor following biopsy or attempted resection, radiation therapy has been reported to achieve local control in 60% to 90% of cases. Because of an increased risk of radiation-induced injury, doses greater than 60 Gy should be avoided. Overall 5-year survival rates of approximately 50% are reported for patients with unresectable stage III tumors. It is uncertain whether patients who undergo tumor debulking have a better prognosis than those who undergo biopsy only.
Chemotherapy: Transient partial responses have been reported with single-agent doxorubicin, maytansine, cisplatin, ifosfamide, and corticosteroids. It is important to remember, however, that corticosteroids and many chemotherapeutic agents are lympholytic; shrinkage of thymic tumors with substantial lymphoid cell infiltration may reflect shrinkage of the nonmalignant components of the tumors rather than the malignant epithelial components.
Combination chemotherapy has been reported to produce both complete and partial remissions.
In a series of 30 patients with stage IV or locally progressive recurrent tumor following radiation therapy, the PAC regimen (cisplatin, doxorubicin, cyclophosphamide) achieved a 50% response rate, including 3 complete responses. The median duration of response was 12 months, and 5-year survival was 32%.In another series, the ADOC regimen (doxorubicin, cisplatin, vincristine, cyclophosphamide) produced a 92% response rate (34 of 37 patients), including complete responses in 43% of patients.
A study of combined chemotherapy with cisplatin and etoposide produced responses in 9 out of 16 patients treated, with a median response duration of 3.4 years and a median survival of 4.3 years. In yet another study, 9 of 28 patients with invasive thymoma or thymic carcinoma who received 4 cycles of etoposide, ifosfamide, and cisplatin at 3-week intervals had partial responses. The median duration of response was 11.9 months (range, <1-26 months), and the median overall survival was 31.6 months. The 1-year and 2-year survival rates were 89% and 70%, respectively.
A retrospective analysis of 17 patients treated with cisplatin alone or in combination with prednisone revealed an overall response rate of 64%.Cisplatin alone (50 mg/m2 every 21 days), however, was associated with a partial response rate of only 10% (2 of 20 patients) in a phase II study. Treatment with single-agent ifosfamide was associated with 5 complete responses and 1 partial response in 13 patients with advanced thymoma in another prospective study.
Neoadjuvant chemotherapy followed by resection: One series of 16 patients with stages III or IVa disease were treated with initial ADOC chemotherapy. All patients achieved a clinical response to chemotherapy. Eleven patients had residual histologic tumor and received postoperative radiation therapy. The median survival of the entire group was 66 months.
Combined chemotherapy and radiation therapy for unresectable tumors. An intergroup study of patients with unresectable disease who received cisplatin, doxorubicin, and cyclophosphamide followed by thoracic radiation reported a 5-year survival rate of 52%.
Recurrent Thymoma and Thymic Carcinoma
Standard treatment options (in order of decreasing effectiveness):
Repeat surgical resection, particularly for local recurrences and, in some cases, pleural and pericardial implants. Postoperative radiation therapy has been used for patients with incomplete resections and has been employed in selected patients following complete resection of recurrent thymoma. Radiation therapy (when possible, based on previous treatment).
Corticosteroids in unresectable tumors that have not responded to radiation therapy.
Chemotherapy: Combination chemotherapy has been reported to produce complete and partial remissions; some of the complete remissions have been pathologically confirmed at subsequent surgery. In a series of 30 patients with stage IV or locally progressive recurrent tumor following radiation therapy, the PAC regimen (cisplatin, doxorubicin, cyclophosphamide) achieved a 50% response rate, including 3 complete responses. The median duration of response was 12 months, and 5-year survival was 32%.
HOW ABOUT THE PROGNOSIS OF THYMOMA AND THYMIC CARCINOMA?
The prognosis of this tumor is related with its staging.It is reported 5-year survival rates of 96% for stage I disease, 86% for stage II disease, 69% for stage III disease, and 50% for stage IV disease. In a large retrospective study involving 273 cases of thymoma, 20-year survival rates (as defined by freedom from tumor death) according to the staging system were reported to be 89% for stage I disease, 91% for stage II disease, 49% for stage III disease, and 0% for stage IV disease.
Thymoma has been associated with an increased risk for second malignancies, which appears to be unrelated to thymectomy, radiation therapy, or a clinical history of myasthenia gravis. Because of this increased risk for second malignancies and the fact that thymoma can recur after a long interval, it has been recommended that surveillance should be lifelong. The measurement of interferon-alpha and interleukin-2 antibodies has been reported to be helpful in identifying patients with a thymoma recurrence.
The thymus is a small organ that lies under the breastbone. It makes white blood cells called lymphocytes that travel through the body and fight infection.
Thymoma and thymic carcinoma are diseases in which cancer (malignant) cells are found in the tissues of the thymus. Thymomas are epithelial tumors of the thymus, which may or may not be extensively infiltrated by nonneoplastic lymphocytes. The term thymoma is customarily used to describe neoplasms that show no overt atypia of the epithelial component. A thymic epithelial tumor that exhibits clear-cut cytologic atypia and histologic features no longer specific to the thymus is known as a thymic carcinoma (also known as type C thymoma).
Invasive thymomas and thymic carcinomas are relatively rare tumors, together representing about 0.2% to 1.5% of all malignancies. Thymic carcinomas are rare and have been reported to account for only 0.06% of all thymic neoplasms. In general, thymomas are indolent tumors with a tendency toward local recurrence rather than metastasis. Thymic carcinomas, however, are typically invasive, with a high risk of relapse and death.
Most patients with thymoma or thymic carcinoma are aged 40 through 60 years. The etiology of these tumors is not known. In about half of cases, thymomas/thymic carcinomas are detected by chance with plain-film chest radiography. Ninety percent occur in the anterior mediastinum.
HOW TO DETECT THYMOMA AND THYMIC CARCINOMA?
Symptoms
The following symptoms suggest thymoma or thymic carcinoma:
A cough that won’t go away.
Pain in the chest.
Weakness in the muscles.
Approximately 30% of patients with thymoma/thymic carcinoma are asymptomatic at the time of diagnosis. In other cases, the presenting clinical signs of these tumors may include coughing, chest pain, and signs of upper airway congestion.
Paraneoplastic autoimmune syndromes associated with thymoma include myasthenia gravis, polymyositis, lupus erythematosus, rheumatoid arthritis, thyroiditis, and Sj?gren’s syndrome, among others. Autoimmune pure red cell aplasia and hypogammaglobulinemia each affect approximately 5% of patients with thymoma.
Thymoma-associated autoimmune disease involves an alteration in circulating T-cell subsets. In addition, B-cell lymphopenia has been observed in thymoma-related immunodeficiency, with hypogammaglobulinemia (Good syndrome) and opportunistic infection. In contrast to thymoma, the association of thymic carcinoma and autoimmune diseases is rare.
Approximately 47% of thymoma cases (excluding thymic carcinoma) were found to be associated with myasthenia gravis.
Stage
Histologic classification of thymoma is not sufficient to distinguish biologically benign thymomas from malignant thymomas. The degree of invasion or tumor stage is generally thought to be a more important indicator of overall survival.
Evaluating the invasiveness of a thymoma involves the use of staging criteria that indicate the presence and degree of contiguous invasion, the presence of implants, and lymph node or distant metastases regardless of histologic type. The following staging system is commonly employed and is shown below.
Thymoma Staging System
Stage
Description
I
Macroscopically, completely encapsulated; microscopically, no capsular invasion
II
Macroscopic invasion into surrounding fatty tissue or mediastinal pleura; microscopic invasion into capsule
III
Macroscopic invasion into neighboring organs (pericardium, lung, great vessels)
IVa
Pleural or pericardial dissemination
IVb
Lymphogenous or hematogenous metastases
For the purposes of treatment, these stages are grouped as either noninvasive or invasive.
Noninvasive
In noninvasive (stage I) disease, the tumor is limited to the thymus gland and has not involved other tissues. All of the tumor cells remain within a fibrous capsule that surrounds the tumor.
Invasive
In locally invasive (stage II) disease, the tumor has broken through the capsule and invaded the fat or pleura. In extensively invasive (stages III and IVa) disease, the tumor has spread contiguously from the thymus gland to involve other organs in the chest. Spread to organs in the abdomen or metastatic embolic spread (stage IVb) is unusual at the time of presentation.
Computed tomography (CT) may be useful in the diagnosis and clinical staging of thymoma, especially for noninvasive tumors. It is usually accurate in predicting tumor size, location, and invasion into vessels, the pericardium, and the lung. It cannot predict, however, invasion or resectability with accuracy. Appearance of the tumor on CT may be related to the World Health Organization histologic type. The smooth contours and a round shape are most suggestive of type A thymomas, whereas irregular contours are most suggestive of thymic carcinomas. Calcification is suggestive of type B thymomas.
HOW TO TREAT THYMOMA AND THYMIC CARCINOMA?
Most thymomas are diagnosed and staged at the time of surgical intervention. Surgical resection is the preferred treatment of patients who can tolerate surgery and have a mediastinal mass that is suspected of being a thymoma. A total thymectomy with complete resection of all tumor can be achieved in nearly all stage I and stage II patients and in 27% to 44% of stage III patients. Postoperative radiation therapy is generally employed for stage II and stage III patients. Patients with stage IVa disease can only rarely be resected completely and are usually offered debulking surgery and postoperative radiation therapy, with or without chemotherapy.
Noninvasive Thymoma and Thymic Carcinoma
Standard treatment options
Surgical resection: Complete resection of a well-encapsulated, noninvasive thymoma is usually curative, with a risk of local recurrence of less than 2%. In patients with myasthenia gravis, operative mortality can be minimized with close attention to respiratory support when planning surgical treatment.
Radiation therapy is not indicated following complete resection of a well-encapsulated thymoma. Radiation therapy should be considered, however, in rare cases when a noninvasive thymoma is incompletely resected, and when the patient is a poor surgical risk.
Invasive Thymoma and Thymic Carcinoma
Operable
En bloc surgical resection if possible. In patients with myasthenia gravis, operative mortality can be minimized with close attention to respiratory support when planning surgical treatment.
Following surgical resection, radiation therapy is generally recommended whether or not the surgical resection has been complete, especially for stage III and stage IVa patients. Retrospective clinical studies show improved local control and survival with the addition of postoperative radiation therapy.
Inoperable (stages III and IV with vena caval obstruction, pleural involvement, pericardial implants, etc.)
Radiation therapy: In patients who have residual macroscopic tumor following biopsy or attempted resection, radiation therapy has been reported to achieve local control in 60% to 90% of cases. Because of an increased risk of radiation-induced injury, doses greater than 60 Gy should be avoided. Overall 5-year survival rates of approximately 50% are reported for patients with unresectable stage III tumors. It is uncertain whether patients who undergo tumor debulking have a better prognosis than those who undergo biopsy only.
Chemotherapy: Transient partial responses have been reported with single-agent doxorubicin, maytansine, cisplatin, ifosfamide, and corticosteroids. It is important to remember, however, that corticosteroids and many chemotherapeutic agents are lympholytic; shrinkage of thymic tumors with substantial lymphoid cell infiltration may reflect shrinkage of the nonmalignant components of the tumors rather than the malignant epithelial components.
Combination chemotherapy has been reported to produce both complete and partial remissions.
In a series of 30 patients with stage IV or locally progressive recurrent tumor following radiation therapy, the PAC regimen (cisplatin, doxorubicin, cyclophosphamide) achieved a 50% response rate, including 3 complete responses. The median duration of response was 12 months, and 5-year survival was 32%.In another series, the ADOC regimen (doxorubicin, cisplatin, vincristine, cyclophosphamide) produced a 92% response rate (34 of 37 patients), including complete responses in 43% of patients.
A study of combined chemotherapy with cisplatin and etoposide produced responses in 9 out of 16 patients treated, with a median response duration of 3.4 years and a median survival of 4.3 years. In yet another study, 9 of 28 patients with invasive thymoma or thymic carcinoma who received 4 cycles of etoposide, ifosfamide, and cisplatin at 3-week intervals had partial responses. The median duration of response was 11.9 months (range, <1-26 months), and the median overall survival was 31.6 months. The 1-year and 2-year survival rates were 89% and 70%, respectively.
A retrospective analysis of 17 patients treated with cisplatin alone or in combination with prednisone revealed an overall response rate of 64%.Cisplatin alone (50 mg/m2 every 21 days), however, was associated with a partial response rate of only 10% (2 of 20 patients) in a phase II study. Treatment with single-agent ifosfamide was associated with 5 complete responses and 1 partial response in 13 patients with advanced thymoma in another prospective study.
Neoadjuvant chemotherapy followed by resection: One series of 16 patients with stages III or IVa disease were treated with initial ADOC chemotherapy. All patients achieved a clinical response to chemotherapy. Eleven patients had residual histologic tumor and received postoperative radiation therapy. The median survival of the entire group was 66 months.
Combined chemotherapy and radiation therapy for unresectable tumors. An intergroup study of patients with unresectable disease who received cisplatin, doxorubicin, and cyclophosphamide followed by thoracic radiation reported a 5-year survival rate of 52%.
Recurrent Thymoma and Thymic Carcinoma
Standard treatment options (in order of decreasing effectiveness):
Repeat surgical resection, particularly for local recurrences and, in some cases, pleural and pericardial implants. Postoperative radiation therapy has been used for patients with incomplete resections and has been employed in selected patients following complete resection of recurrent thymoma. Radiation therapy (when possible, based on previous treatment).
Corticosteroids in unresectable tumors that have not responded to radiation therapy.
Chemotherapy: Combination chemotherapy has been reported to produce complete and partial remissions; some of the complete remissions have been pathologically confirmed at subsequent surgery. In a series of 30 patients with stage IV or locally progressive recurrent tumor following radiation therapy, the PAC regimen (cisplatin, doxorubicin, cyclophosphamide) achieved a 50% response rate, including 3 complete responses. The median duration of response was 12 months, and 5-year survival was 32%.
HOW ABOUT THE PROGNOSIS OF THYMOMA AND THYMIC CARCINOMA?
The prognosis of this tumor is related with its staging.It is reported 5-year survival rates of 96% for stage I disease, 86% for stage II disease, 69% for stage III disease, and 50% for stage IV disease. In a large retrospective study involving 273 cases of thymoma, 20-year survival rates (as defined by freedom from tumor death) according to the staging system were reported to be 89% for stage I disease, 91% for stage II disease, 49% for stage III disease, and 0% for stage IV disease.
Thymoma has been associated with an increased risk for second malignancies, which appears to be unrelated to thymectomy, radiation therapy, or a clinical history of myasthenia gravis. Because of this increased risk for second malignancies and the fact that thymoma can recur after a long interval, it has been recommended that surveillance should be lifelong. The measurement of interferon-alpha and interleukin-2 antibodies has been reported to be helpful in identifying patients with a thymoma recurrence.
Testicular Cancer
WHAT IS TESTICULAR CANCER?
Testicular cancer is a disease in which malignant (cancer) cells form in the tissues of one or both testicles.
The testicles are 2 egg-shaped glands located inside the scrotum (a sac of loose skin that lies directly below the penis). The testicles are held within the scrotum by the spermatic cord, which also contains the vas deferens and vessels and nerves of the testicles.
The testicles are the male sex glands and produce testosterone and sperm. Germ cells within the testicles produce immature sperm that travel through a network of tubules (tiny tubes) and larger tubes into the epididymis (a long coiled tube next to the testicles) where the sperm mature and are stored.
Almost all testicular cancers start in the germ cells. The two main types of testicular germ cell tumors are seminomas and nonseminomas. These 2 types grow and spread differently and are treated differently. Nonseminomas tend to grow and spread more quickly than seminomas. Seminomas are more sensitive to radiation. A testicular tumor that contains both seminoma and nonseminoma cells is treated as a nonseminoma.
Testicular cancer is the most common cancer in men 20 to 35 years old.
WHAT ARE THE RISK FACTORS OF TESTICULAR CANCER?
Health history can affect the risk of developing testicular cancer. Risk factors for testicular cancer include:
Having had an undescended testicle.
Having had abnormal development of the testicles.
Having a personal or family history of testicular cancer.
Having Klinefelter's syndrome.
Being white.
HOW TO DETECT TESTICULAR CANCER?
Possible signs of testicular cancer include swelling or discomfort in the scrotum.
A painless lump or swelling in either testicle.
A change in how the testicle feels.
A dull ache in the lower abdomen or the groin.
A sudden build-up of fluid in the scrotum.
Pain or discomfort in a testicle or in the scrotum.
Tests that examine the testicles and blood are used to detect (find) and diagnose testicular cancer.
The following tests and procedures may be used:
Physical exam and history: The testicles will be examined to check for lumps, swelling, or pain.
Ultrasound test will be used to check for abnormal sonogram of testicles.
Serum tumor marker test: The following 3 tumor markers are used to detect testicular cancer:
Alpha-fetoprotein (AFP).
Beta-human chorionic gonadotropin (β-hCG).
Lactate dehydrogenase (LDH).
Tumor marker levels are measured before radical inguinal orchiectomy and biopsy, to help diagnose testicular cancer.
Radical inguinal orchiectomy and biopsy: A procedure to remove the entire testicle through an incision in the groin. A tissue sample from the testicle is then viewed under a microscope to check for cancer cells. If cancer is found, the cell type (seminoma or nonseminoma) is determined in order to help plan treatment.
Testicular cancer is broadly divided into seminoma and nonseminoma types
Types are very important for treatment planning because seminomas are more sensitive to radiation therapy. For patients with seminoma (all stages combined), the cure rate exceeds 90%. For patients with low-stage disease, the cure rate approaches 100%.
Tumors which have a mixture of seminoma and nonseminoma components should be managed as nonseminoma. Nonseminoma includes embryonal carcinoma, teratoma, yolk sac carcinoma and choriocarcinoma, and various combinations of these cell types. Tumors that appear to have a seminoma histology but that have elevated serum levels of alpha fetoprotein (AFP) should be treated as nonseminomas. Elevation of the beta subunit of human chorionic gonadotropin (HCG) alone is found in approximately 10% of patients with pure seminoma.
Risk of metastases is lowest for teratoma and highest for choriocarcinoma, with the other cell types being intermediate.
Stage Information
The American Joint Committee on Cancer (AJCC) has designated staging by TNM classification.
Primary tumor (T)
The extent of primary tumor is classified after radical orchiectomy, and for this reason, a pathologic stage is assigned.
pTX: Primary tumor cannot be assessed*
pT0: No evidence of primary tumor (e.g., histologic scar in testis)
pTis: Intratubular germ cell neoplasia (carcinoma in situ)
pT1: Tumor limited to the testis and epididymis without lymphatic/vascular invasion; tumor may invade into the tunica albuginea but not the tunica vaginalis
pT2: Tumor limited to the testis and epididymis with vascular/lymphatic invasion, or tumor extending through the tunica albuginea with involvement of the tunica vaginalis
pT3: Tumor invades the spermatic cord with or without vascular/lymphatic invasion
pT4: Tumor invades the scrotum with or without vascular/lymphatic invasion
* [Note: Except for pTis and pT4, extent of primary tumor is classified by radical orchiectomy. TX may be used for other categories in the absence of radical orchiectomy.]
Regional lymph nodes (N)
NX: Regional lymph nodes cannot be assessed
N0: No regional lymph node metastasis
N1: Metastasis with a single lymph node mass 2 cm or less in greatest dimension; or multiple lymph nodes, none more than 2 cm in greatest dimension
N2: Metastasis with a single lymph node mass more than 2 cm but not more than 5 cm in greatest dimension; or multiple lymph nodes, none more than 5 cm in greatest dimension
N3: Metastasis with a lymph node mass more than 5 cm in greatest dimension
Distant metastasis (M)
MX: Presence of distant metastasis cannot be assessed
M0: No distant metastasis
M1: Distant metastasis
M1a: Non-regional nodal or pulmonary metastasis
M1b: Distant metastasis other than to non-regional lymph nodes and lungs
Serum tumor markers (S)
SX: Marker studies not available or not performed
S0: Marker study levels within normal limits
S1: LDH < 1.5 X N* AND
hCG (mIu/ml) < 5000 AND
AFP (ng/ml) < 1000
S2: LDH 1.5-10 X N* OR
hCG (mIu/ml) 5000-50,000 OR
AFP (ng/ml) 1000-10,000
S3: LDH > 10 X N* OR
hCG (mIu/ml) > 50,000 OR
AFP (ng/ml) > 10,000
* [Note: N indicates the upper limit of normal for the LDH assay.]
AJCC stage groupings
Stage 0
pTis, N0, M0, S0
Stage I
pT1-4, N0, M0, SX
Stage IA
pT1, N0, M0, S0
Stage IB
pT2, N0, M0, S0
pT3, N0, M0, S0
pT4, N0, M0, S0
Stage IS
Any pT/Tx, N0, M0, S1-3
Stage II
Any pT/Tx, N1-3, M0, SX
Stage IIA
Any pT/Tx, N1, M0, S0
Any pT/Tx, N1, M0, S1
Stage IIB
Any pT/Tx, N2, M0, S0
Any pT/Tx, N2, M0, S1
Stage IIC
Any pT/Tx, N3, M0, S0
Any pT/Tx, N3, M0, S1
Stage III
Any pT/Tx, any N, M1, SX
Stage IIIA
Any pT/Tx, any N, M1a, S0
Any pT/Tx, any N, M1a, S1
Stage IIIB
Any pT/Tx, N1-3, M0, S2
Any pT/Tx, any N, M1a, S2
Stage IIIC
Any pT/Tx, N1-3, M0, S3
Any pT/Tx, any N, M1a, S3
Any pT/Tx, any N, M1b, any S
Surgical stage
In addition to the clinical stage definitions, surgical stage may be designated based on the results of surgical removal and microscopic examination of tissue.
Stage I
Stage I testicular cancer is limited to the testis. Invasion of the scrotal wall by tumor or interruption of the scrotal wall by previous surgery does not change the stage but does increase the risk of spread to the inguinal lymph nodes, and this must be considered in treatment and follow-up. Invasion of the epididymis tunica albuginea and/or the spermatic cord also does not change the stage but does increase the risk of retroperitoneal nodal involvement and the risk of recurrence. This stage corresponds to AJCC stages I and II.
Stage II
Stage II testicular cancer involves the testis and the retroperitoneal or para-aortic lymph nodes usually in the region of the kidney. Retroperitoneal involvement should be further characterized by the number of nodes involved and the size of involved nodes. The risk of recurrence is increased if more than 5 nodes are involved, if the size of 1 or more involved nodes is larger than 2 centimeters, or if there is extranodal fat involvement. Bulky stage II disease describes patients with extensive retroperitoneal nodes (>5 centimeters) who require primary chemotherapy and who have a less favorable prognosis. This stage corresponds to AJCC stages III and IV (no distant metastasis).
Stage III
Stage III implies spread beyond the retroperitoneal nodes based on physical examination, x-rays, and/or blood tests. Stage III is subdivided into nonbulky stage III versus bulky stage III. In nonbulky stage III, metastases are limited to lymph nodes and lung with no mass larger than 2 centimeters in diameter. Bulky stage III includes extensive retroperitoneal nodal involvement, plus lung nodules or spread to other organs such as liver or brain. This stage corresponds to AJCC stage IV (distant metastasis).
HOW TO TREAT TESTICULAR CANCER?
Testicular cancer is broadly divided into seminoma and nonseminoma for treatment planning because seminomatous types of testicular cancer are more sensitive to radiation therapy. Nonseminomatous testicular tumors include yolk sac tumors.
Stage I Testicular Cancer
Stage I seminoma
Stage I seminoma has a cure rate of greater than 95%.
Radical inguinal orchiectomy-radiation therapy：Removal of the testicle via radical inguinal orchiectomy followed by radiation therapy. Prophylactic irradiation of the retroperitoneal nodes will be performed even with a negative lymphangiogram and/or computed tomographic (CT) scan because approximately 15% of patients will have occult nodal spread that can be cured with irradiation. Patients with tumors with vascular invasion seem at higher risk for nodal metastases.
Radical inguinal orchiectomywith no retroperitoneal node irradiation: Postorchiectomy surveillance should be performed with determination of serum markers, chest x-rays, and CT scans. Patients whose disease recurred will receive radiation therapy or chemotherapy. The overall cure rate is often indistinguishable from that achieved with adjuvant radiation therapy. The size of the primary tumors may be a prognostic factor, as the patients with tumors larger than 6 centimeters have a higher risk of relapse.
Stage I nonseminoma
Stage I nonseminoma is highly curable (>95%). If preservation of fertility is an important consideration, a surgical technique for sparing sympathetic ganglia and chains should be used. This technique is associated with postoperative fertility in most patients and appears to be as effective as non-nerve-sparing procedures in preventing retroperitoneal relapse.
Removal of the testicle through the groin followed (in adults) by retroperitoneal lymph node dissection. A nerve-sparing retroperitoneal lymphadenectomy (RPL) that preserves ejaculation in virtually every patient has been described in clinical stage I patients and appears to be as effective as the standard RPL dissection. Surgery should be followed by monthly determination of serum markers and chest x-rays for the first year and 1 to 2 month determinations the second year. In patients with pathologic stage I disease after RPL, the presence of lymphatic or venous invasion in the primary tumor appears to predict for relapse. Chemotherapy is employed immediately on first evidence of recurrence.
Radical inguinal orchiectomy with no retroperitoneal node dissection followed by regular (e.g., every 1-2 months) history, physical examination, determination of serum markers, and, during the first year, abdominal CT scan (surveillance). Intervals for abdominal CT scans have varied from every 2 months to scans at 3 and 12 months postorchiectomy, with apparently similar outcomes. Disease recurrence is rarely detected by chest x-ray alone, so chest x-ray may play little or no role in routine surveillance. Long-term follow-up is important, since relapses have been reported more than 5 years after the orchiectomy in patients who did not undergo a retroperitoneal dissection.
Stage II Testicular Cancer
Stage II seminoma
Stage II seminoma is divided into bulky and nonbulky disease for treatment planning and expression of prognosis. Bulky disease is generally defined as tumors greater than 5 centimeters on a computed tomographic (CT) scan.
For patients with nonbulky tumors
Radical inguinal orchiectomy followed by radiation to the retroperitoneal and ipsilateral pelvic lymph nodes. Evidence favors the omission of prophylactic radiation therapy to the mediastinum and neck. Radiation to inguinal nodes is not standard unless there has been some damage to the scrotum to put inguinal lymph nodes at risk.
For patients with bulky tumors
Radical inguinal orchiectomy followed by combination chemotherapy (with a cisplatin-based regimen), or by radiation to the abdominal and pelvic lymph nodes. Recurrence rate is higher after radiation for bulky stage II tumors than radiation for nonbulky tumors, leading some authors to recommend primary chemotherapy for patients with bulky disease (>/= 5-10 centimeters).
Stage II nonseminoma
Stage II nonseminoma is highly curable (>95%). If preservation of fertility is an important consideration, surgical techniques for sparing sympathetic ganglia and chains without compromising the total removal of all involved nodes are available, although this technique may not be feasible in many patients. In most patients, an orchiectomy is performed prior to starting chemotherapy.
Radical inguinal orchiectomy followed by removal of retroperitoneal lymph nodes with or without fertility-preserving RPL followed by monthly checkups, which include physical examination, chest x-ray, and serum marker tests (alpha fetoprotein, human chorionic gonadotropin, and lactate dehydrogenase). This option of surgery and careful follow-up, reserving chemotherapy for relapse, is particularly attractive for patients who have less than 6 positive nodes at retroperitoneal lymph node dissection, none of which are greater than 2 centimeters in diameter, and no extracapsular lymph node invasion.
Radical inguinal orchiectomy followed by removal of retroperitoneal lymph nodes followed by chemotherapy and then monthly checkups. Two courses of cisplatin-based chemotherapy (either cisplatin, vinblastine, bleomycin (PVB) or vinblastine, dactinomycin, bleomycin, cyclophosphamide, cisplatin (VAB VI)) prevented a relapse in greater than 95% of patients.
Radical inguinal orchiectomy followed by chemotherapy with delayed surgery for removal of residual masses (if present) followed by monthly checkups. This option would be considered for patients in whom clinical examination, lymphangiogram, or CT scan show large enough retroperitoneal masses that there are concerns about resectability.
Chemotherapy regimens include:
BEP: bleomycin + etoposide + cisplatin for 3 courses. A modified regimen has been used in children.
EP: etoposide + cisplatin for 4 courses in good-prognosis patients.
A randomized study has shown that bleomycin is an essential component of the BEP regimen when only 3 courses are administered.
Other regimens that appear to produce similar survival outcomes but are in less common use include:
PVB: cisplatin + vinblastine + bleomycin.
VAB VI: vinblastine + dactinomycin + bleomycin + cyclophosphamide + cisplatin.
VPV: vinblastine + cisplatin + etoposide.
Stage III Testicular Cancer
Stage III seminoma
Stage III seminoma is usually curable.
Radical inguinal orchiectomy followed by multidrug chemotherapy. In seminoma patients, the residual masses after chemotherapy are often fibrotic, although persistent, discrete (large) masses (>/= 3 centimeters) that may contain residual seminoma that would require additional therapy. In some patients, fertility has been returned following the use of bleomycin, etoposide, and cisplatin (BEP).
Chemotherapy combinations include:
BEP: bleomycin + etoposide + cisplatin. A modified regimen has been used in children.
EP: etoposide + cisplatin for 4 courses in good-prognosis patients.
Other regimens that appear to produce similar survival outcomes but are in less common use include:
PVB: cisplatin + vinblastine + bleomycin.
VIP: etoposide + ifosfamide + cisplatin.
Stage III nonseminoma
Stage III nonseminoma is usually curable (70%) with standard chemotherapy. In some patients fertility has returned following the use of chemotherapy. The 30% of patients who are not cured with standard chemotherapy usually have widespread visceral metastases, high tumor markers, or mediastinal primary tumors at presentation. In most patients, an orchiectomy is performed prior to starting chemotherapy.
Chemotherapy
BEP: bleomycin + etoposide + cisplatin. A modified regimen has been used in children.
EP: etoposide + cisplatin for 4 courses in good-prognosis patients.
Other regimens that appear to produce similar survival outcomes but have been studied less extensively or are in less common use include:
PVB: cisplatin + vinblastine + bleomycin.
POMB/ACE: platinum + vincristine + methotrexate + bleomycin + dactinomycin + cyclophosphamide + etoposide.
VIP: etoposide + ifosfamide + cisplatin.
A randomized study comparing 4 courses of BEP to 4 courses of VIP showed similar overall survival and time-to-treatment failure for the 2 regimens in patients with advanced disseminated germ cell tumors who had not received prior chemotherapy. Hematologic toxic effects were substantially worse with the VIP regimen.
Recurrent Testicular Cancer
Salvage regimens consisting of ifosfamide, cisplatin, and either etoposide or vinblastine can induce long-term complete responses in about one-quarter of patients with disease that has persisted or recurred following other cisplatin-based regimens. Patients who have had an initial complete response to first-line chemotherapy and those without extensive disease have the most favorable outcomes. This regimen is now the standard initial salvage regimen.
High-dose chemotherapy with autologous marrow transplantation has also been used with some success in the setting of refractory disease. Durable complete remissions may be achieved in 10% to 20% of patients with disease resistant to standard cisplatin-based regimens who are treated with high-dose carboplatin and etoposide with autologous bone marrow transplantation. The durable complete remission rate may exceed 50% if high-dose chemotherapy is used as salvage chemotherapy at the initial relapse of primary testicular cancer.
HOW TO DETECT THE PROGNOSIS OF TESTICULAR CARCINOMA?
The following factors affect prognosis (chance of recovery) of this cancer.
Stage of the cancer (whether it is in or near the testicle or has spread to other places in the body, and blood levels of AFP, β-hCG, and LDH).
Type of cancer.
Size of the tumor.
Number and size of retroperitoneal lymph nodes.
Testicular cancer is a highly treatable, often curable cancer. Some or all of the following factors may independently predict worse prognosis:
Presence of liver, bone, or brain metastases.
Very high serum markers.
Primary mediastinal nonseminoma.
Large number of lung metastases.
It is important to note that even patients with widespread metastases at presentation, including those with brain metastases, may still be curable and should be treated with this intent.
An important aspect of the follow-up of testicular cancer is the use of serum markers. Serum markers include AFP, HCG (measurement of the beta subunit reduces luteinizing hormone (LH) cross-reactivity), and lactate dehydrogenase (LDH). They may detect a tumor which is too small to be detected on physical examination or x-rays. Patients typically receive follow-up monthly for the first year and every other month for the second year after diagnosis and treatment. While the majority of tumor recurrences appear within 2 years, late relapse has been reported and lifelong marker, radiologic, and physical examination is recommended.
Patients who have been cured of testicular cancer have approximately a 2% to 5% cumulative risk of developing a cancer in the opposite testicle over the 25 years after initial diagnosis.
Good Prognosis
Nonseminoma:
Testis/retroperitoneal primary AND
No non-pulmonary visceral metastases AND
Good markers - all of:
AFP < 1000 ng/ml AND
hCG < 5000 iu/l (1000 ng/ml) AND
LDH < 1.5 x upper limit of normal
56% of nonseminomas
5-year progression-free survival (PFS) 89%; 5-year survival 92%
Seminoma:
Any primary site AND
No non-pulmonary visceral metastases AND
Normal AFP, any hCG, any LDH
90% of seminomas
5-year PFS 82%; 5-year survival 86%
Intermediate Prognosis
Nonseminoma:
Testis/retroperitoneal primary AND
No non-pulmonary visceral metastases AND
Intermediate markers - any of:
AFP >/= 1000 and hCG >/= 5000 iu/l and LDH >/= 1.5 x N* and 28% of nonseminomas
5-year PFS 75%; 5-year survival 80%
[Note: N indicates the upper limit of normal for the LDH assay.]
Seminoma:
Any primary site AND
Non-pulmonary visceral metastases AND
Normal AFP, any hCG, any LDH
10% of seminomas
5-year PFS 67%; 5-year survival 72%
Poor Prognosis
Nonseminoma:
Mediastinal primary OR
Non-pulmonary visceral metastases OR
For markers - any of:
AFP > 10,000 ng/ml OR
hCG > 50,000 iu/l (10,000 ng/ml) OR
LDH > 10 x upper limit of normal
16% of nonseminomas
5-year PFS 41%; 5-year survival 48%
Seminoma:
No patients classified as poor prognosis.
Testicular cancer is a disease in which malignant (cancer) cells form in the tissues of one or both testicles.
The testicles are 2 egg-shaped glands located inside the scrotum (a sac of loose skin that lies directly below the penis). The testicles are held within the scrotum by the spermatic cord, which also contains the vas deferens and vessels and nerves of the testicles.
The testicles are the male sex glands and produce testosterone and sperm. Germ cells within the testicles produce immature sperm that travel through a network of tubules (tiny tubes) and larger tubes into the epididymis (a long coiled tube next to the testicles) where the sperm mature and are stored.
Almost all testicular cancers start in the germ cells. The two main types of testicular germ cell tumors are seminomas and nonseminomas. These 2 types grow and spread differently and are treated differently. Nonseminomas tend to grow and spread more quickly than seminomas. Seminomas are more sensitive to radiation. A testicular tumor that contains both seminoma and nonseminoma cells is treated as a nonseminoma.
Testicular cancer is the most common cancer in men 20 to 35 years old.
WHAT ARE THE RISK FACTORS OF TESTICULAR CANCER?
Health history can affect the risk of developing testicular cancer. Risk factors for testicular cancer include:
Having had an undescended testicle.
Having had abnormal development of the testicles.
Having a personal or family history of testicular cancer.
Having Klinefelter's syndrome.
Being white.
HOW TO DETECT TESTICULAR CANCER?
Possible signs of testicular cancer include swelling or discomfort in the scrotum.
A painless lump or swelling in either testicle.
A change in how the testicle feels.
A dull ache in the lower abdomen or the groin.
A sudden build-up of fluid in the scrotum.
Pain or discomfort in a testicle or in the scrotum.
Tests that examine the testicles and blood are used to detect (find) and diagnose testicular cancer.
The following tests and procedures may be used:
Physical exam and history: The testicles will be examined to check for lumps, swelling, or pain.
Ultrasound test will be used to check for abnormal sonogram of testicles.
Serum tumor marker test: The following 3 tumor markers are used to detect testicular cancer:
Alpha-fetoprotein (AFP).
Beta-human chorionic gonadotropin (β-hCG).
Lactate dehydrogenase (LDH).
Tumor marker levels are measured before radical inguinal orchiectomy and biopsy, to help diagnose testicular cancer.
Radical inguinal orchiectomy and biopsy: A procedure to remove the entire testicle through an incision in the groin. A tissue sample from the testicle is then viewed under a microscope to check for cancer cells. If cancer is found, the cell type (seminoma or nonseminoma) is determined in order to help plan treatment.
Testicular cancer is broadly divided into seminoma and nonseminoma types
Types are very important for treatment planning because seminomas are more sensitive to radiation therapy. For patients with seminoma (all stages combined), the cure rate exceeds 90%. For patients with low-stage disease, the cure rate approaches 100%.
Tumors which have a mixture of seminoma and nonseminoma components should be managed as nonseminoma. Nonseminoma includes embryonal carcinoma, teratoma, yolk sac carcinoma and choriocarcinoma, and various combinations of these cell types. Tumors that appear to have a seminoma histology but that have elevated serum levels of alpha fetoprotein (AFP) should be treated as nonseminomas. Elevation of the beta subunit of human chorionic gonadotropin (HCG) alone is found in approximately 10% of patients with pure seminoma.
Risk of metastases is lowest for teratoma and highest for choriocarcinoma, with the other cell types being intermediate.
Stage Information
The American Joint Committee on Cancer (AJCC) has designated staging by TNM classification.
Primary tumor (T)
The extent of primary tumor is classified after radical orchiectomy, and for this reason, a pathologic stage is assigned.
pTX: Primary tumor cannot be assessed*
pT0: No evidence of primary tumor (e.g., histologic scar in testis)
pTis: Intratubular germ cell neoplasia (carcinoma in situ)
pT1: Tumor limited to the testis and epididymis without lymphatic/vascular invasion; tumor may invade into the tunica albuginea but not the tunica vaginalis
pT2: Tumor limited to the testis and epididymis with vascular/lymphatic invasion, or tumor extending through the tunica albuginea with involvement of the tunica vaginalis
pT3: Tumor invades the spermatic cord with or without vascular/lymphatic invasion
pT4: Tumor invades the scrotum with or without vascular/lymphatic invasion
* [Note: Except for pTis and pT4, extent of primary tumor is classified by radical orchiectomy. TX may be used for other categories in the absence of radical orchiectomy.]
Regional lymph nodes (N)
NX: Regional lymph nodes cannot be assessed
N0: No regional lymph node metastasis
N1: Metastasis with a single lymph node mass 2 cm or less in greatest dimension; or multiple lymph nodes, none more than 2 cm in greatest dimension
N2: Metastasis with a single lymph node mass more than 2 cm but not more than 5 cm in greatest dimension; or multiple lymph nodes, none more than 5 cm in greatest dimension
N3: Metastasis with a lymph node mass more than 5 cm in greatest dimension
Distant metastasis (M)
MX: Presence of distant metastasis cannot be assessed
M0: No distant metastasis
M1: Distant metastasis
M1a: Non-regional nodal or pulmonary metastasis
M1b: Distant metastasis other than to non-regional lymph nodes and lungs
Serum tumor markers (S)
SX: Marker studies not available or not performed
S0: Marker study levels within normal limits
S1: LDH < 1.5 X N* AND
hCG (mIu/ml) < 5000 AND
AFP (ng/ml) < 1000
S2: LDH 1.5-10 X N* OR
hCG (mIu/ml) 5000-50,000 OR
AFP (ng/ml) 1000-10,000
S3: LDH > 10 X N* OR
hCG (mIu/ml) > 50,000 OR
AFP (ng/ml) > 10,000
* [Note: N indicates the upper limit of normal for the LDH assay.]
AJCC stage groupings
Stage 0
pTis, N0, M0, S0
Stage I
pT1-4, N0, M0, SX
Stage IA
pT1, N0, M0, S0
Stage IB
pT2, N0, M0, S0
pT3, N0, M0, S0
pT4, N0, M0, S0
Stage IS
Any pT/Tx, N0, M0, S1-3
Stage II
Any pT/Tx, N1-3, M0, SX
Stage IIA
Any pT/Tx, N1, M0, S0
Any pT/Tx, N1, M0, S1
Stage IIB
Any pT/Tx, N2, M0, S0
Any pT/Tx, N2, M0, S1
Stage IIC
Any pT/Tx, N3, M0, S0
Any pT/Tx, N3, M0, S1
Stage III
Any pT/Tx, any N, M1, SX
Stage IIIA
Any pT/Tx, any N, M1a, S0
Any pT/Tx, any N, M1a, S1
Stage IIIB
Any pT/Tx, N1-3, M0, S2
Any pT/Tx, any N, M1a, S2
Stage IIIC
Any pT/Tx, N1-3, M0, S3
Any pT/Tx, any N, M1a, S3
Any pT/Tx, any N, M1b, any S
Surgical stage
In addition to the clinical stage definitions, surgical stage may be designated based on the results of surgical removal and microscopic examination of tissue.
Stage I
Stage I testicular cancer is limited to the testis. Invasion of the scrotal wall by tumor or interruption of the scrotal wall by previous surgery does not change the stage but does increase the risk of spread to the inguinal lymph nodes, and this must be considered in treatment and follow-up. Invasion of the epididymis tunica albuginea and/or the spermatic cord also does not change the stage but does increase the risk of retroperitoneal nodal involvement and the risk of recurrence. This stage corresponds to AJCC stages I and II.
Stage II
Stage II testicular cancer involves the testis and the retroperitoneal or para-aortic lymph nodes usually in the region of the kidney. Retroperitoneal involvement should be further characterized by the number of nodes involved and the size of involved nodes. The risk of recurrence is increased if more than 5 nodes are involved, if the size of 1 or more involved nodes is larger than 2 centimeters, or if there is extranodal fat involvement. Bulky stage II disease describes patients with extensive retroperitoneal nodes (>5 centimeters) who require primary chemotherapy and who have a less favorable prognosis. This stage corresponds to AJCC stages III and IV (no distant metastasis).
Stage III
Stage III implies spread beyond the retroperitoneal nodes based on physical examination, x-rays, and/or blood tests. Stage III is subdivided into nonbulky stage III versus bulky stage III. In nonbulky stage III, metastases are limited to lymph nodes and lung with no mass larger than 2 centimeters in diameter. Bulky stage III includes extensive retroperitoneal nodal involvement, plus lung nodules or spread to other organs such as liver or brain. This stage corresponds to AJCC stage IV (distant metastasis).
HOW TO TREAT TESTICULAR CANCER?
Testicular cancer is broadly divided into seminoma and nonseminoma for treatment planning because seminomatous types of testicular cancer are more sensitive to radiation therapy. Nonseminomatous testicular tumors include yolk sac tumors.
Stage I Testicular Cancer
Stage I seminoma
Stage I seminoma has a cure rate of greater than 95%.
Radical inguinal orchiectomy-radiation therapy：Removal of the testicle via radical inguinal orchiectomy followed by radiation therapy. Prophylactic irradiation of the retroperitoneal nodes will be performed even with a negative lymphangiogram and/or computed tomographic (CT) scan because approximately 15% of patients will have occult nodal spread that can be cured with irradiation. Patients with tumors with vascular invasion seem at higher risk for nodal metastases.
Radical inguinal orchiectomywith no retroperitoneal node irradiation: Postorchiectomy surveillance should be performed with determination of serum markers, chest x-rays, and CT scans. Patients whose disease recurred will receive radiation therapy or chemotherapy. The overall cure rate is often indistinguishable from that achieved with adjuvant radiation therapy. The size of the primary tumors may be a prognostic factor, as the patients with tumors larger than 6 centimeters have a higher risk of relapse.
Stage I nonseminoma
Stage I nonseminoma is highly curable (>95%). If preservation of fertility is an important consideration, a surgical technique for sparing sympathetic ganglia and chains should be used. This technique is associated with postoperative fertility in most patients and appears to be as effective as non-nerve-sparing procedures in preventing retroperitoneal relapse.
Removal of the testicle through the groin followed (in adults) by retroperitoneal lymph node dissection. A nerve-sparing retroperitoneal lymphadenectomy (RPL) that preserves ejaculation in virtually every patient has been described in clinical stage I patients and appears to be as effective as the standard RPL dissection. Surgery should be followed by monthly determination of serum markers and chest x-rays for the first year and 1 to 2 month determinations the second year. In patients with pathologic stage I disease after RPL, the presence of lymphatic or venous invasion in the primary tumor appears to predict for relapse. Chemotherapy is employed immediately on first evidence of recurrence.
Radical inguinal orchiectomy with no retroperitoneal node dissection followed by regular (e.g., every 1-2 months) history, physical examination, determination of serum markers, and, during the first year, abdominal CT scan (surveillance). Intervals for abdominal CT scans have varied from every 2 months to scans at 3 and 12 months postorchiectomy, with apparently similar outcomes. Disease recurrence is rarely detected by chest x-ray alone, so chest x-ray may play little or no role in routine surveillance. Long-term follow-up is important, since relapses have been reported more than 5 years after the orchiectomy in patients who did not undergo a retroperitoneal dissection.
Stage II Testicular Cancer
Stage II seminoma
Stage II seminoma is divided into bulky and nonbulky disease for treatment planning and expression of prognosis. Bulky disease is generally defined as tumors greater than 5 centimeters on a computed tomographic (CT) scan.
For patients with nonbulky tumors
Radical inguinal orchiectomy followed by radiation to the retroperitoneal and ipsilateral pelvic lymph nodes. Evidence favors the omission of prophylactic radiation therapy to the mediastinum and neck. Radiation to inguinal nodes is not standard unless there has been some damage to the scrotum to put inguinal lymph nodes at risk.
For patients with bulky tumors
Radical inguinal orchiectomy followed by combination chemotherapy (with a cisplatin-based regimen), or by radiation to the abdominal and pelvic lymph nodes. Recurrence rate is higher after radiation for bulky stage II tumors than radiation for nonbulky tumors, leading some authors to recommend primary chemotherapy for patients with bulky disease (>/= 5-10 centimeters).
Stage II nonseminoma
Stage II nonseminoma is highly curable (>95%). If preservation of fertility is an important consideration, surgical techniques for sparing sympathetic ganglia and chains without compromising the total removal of all involved nodes are available, although this technique may not be feasible in many patients. In most patients, an orchiectomy is performed prior to starting chemotherapy.
Radical inguinal orchiectomy followed by removal of retroperitoneal lymph nodes with or without fertility-preserving RPL followed by monthly checkups, which include physical examination, chest x-ray, and serum marker tests (alpha fetoprotein, human chorionic gonadotropin, and lactate dehydrogenase). This option of surgery and careful follow-up, reserving chemotherapy for relapse, is particularly attractive for patients who have less than 6 positive nodes at retroperitoneal lymph node dissection, none of which are greater than 2 centimeters in diameter, and no extracapsular lymph node invasion.
Radical inguinal orchiectomy followed by removal of retroperitoneal lymph nodes followed by chemotherapy and then monthly checkups. Two courses of cisplatin-based chemotherapy (either cisplatin, vinblastine, bleomycin (PVB) or vinblastine, dactinomycin, bleomycin, cyclophosphamide, cisplatin (VAB VI)) prevented a relapse in greater than 95% of patients.
Radical inguinal orchiectomy followed by chemotherapy with delayed surgery for removal of residual masses (if present) followed by monthly checkups. This option would be considered for patients in whom clinical examination, lymphangiogram, or CT scan show large enough retroperitoneal masses that there are concerns about resectability.
Chemotherapy regimens include:
BEP: bleomycin + etoposide + cisplatin for 3 courses. A modified regimen has been used in children.
EP: etoposide + cisplatin for 4 courses in good-prognosis patients.
A randomized study has shown that bleomycin is an essential component of the BEP regimen when only 3 courses are administered.
Other regimens that appear to produce similar survival outcomes but are in less common use include:
PVB: cisplatin + vinblastine + bleomycin.
VAB VI: vinblastine + dactinomycin + bleomycin + cyclophosphamide + cisplatin.
VPV: vinblastine + cisplatin + etoposide.
Stage III Testicular Cancer
Stage III seminoma
Stage III seminoma is usually curable.
Radical inguinal orchiectomy followed by multidrug chemotherapy. In seminoma patients, the residual masses after chemotherapy are often fibrotic, although persistent, discrete (large) masses (>/= 3 centimeters) that may contain residual seminoma that would require additional therapy. In some patients, fertility has been returned following the use of bleomycin, etoposide, and cisplatin (BEP).
Chemotherapy combinations include:
BEP: bleomycin + etoposide + cisplatin. A modified regimen has been used in children.
EP: etoposide + cisplatin for 4 courses in good-prognosis patients.
Other regimens that appear to produce similar survival outcomes but are in less common use include:
PVB: cisplatin + vinblastine + bleomycin.
VIP: etoposide + ifosfamide + cisplatin.
Stage III nonseminoma
Stage III nonseminoma is usually curable (70%) with standard chemotherapy. In some patients fertility has returned following the use of chemotherapy. The 30% of patients who are not cured with standard chemotherapy usually have widespread visceral metastases, high tumor markers, or mediastinal primary tumors at presentation. In most patients, an orchiectomy is performed prior to starting chemotherapy.
Chemotherapy
BEP: bleomycin + etoposide + cisplatin. A modified regimen has been used in children.
EP: etoposide + cisplatin for 4 courses in good-prognosis patients.
Other regimens that appear to produce similar survival outcomes but have been studied less extensively or are in less common use include:
PVB: cisplatin + vinblastine + bleomycin.
POMB/ACE: platinum + vincristine + methotrexate + bleomycin + dactinomycin + cyclophosphamide + etoposide.
VIP: etoposide + ifosfamide + cisplatin.
A randomized study comparing 4 courses of BEP to 4 courses of VIP showed similar overall survival and time-to-treatment failure for the 2 regimens in patients with advanced disseminated germ cell tumors who had not received prior chemotherapy. Hematologic toxic effects were substantially worse with the VIP regimen.
Recurrent Testicular Cancer
Salvage regimens consisting of ifosfamide, cisplatin, and either etoposide or vinblastine can induce long-term complete responses in about one-quarter of patients with disease that has persisted or recurred following other cisplatin-based regimens. Patients who have had an initial complete response to first-line chemotherapy and those without extensive disease have the most favorable outcomes. This regimen is now the standard initial salvage regimen.
High-dose chemotherapy with autologous marrow transplantation has also been used with some success in the setting of refractory disease. Durable complete remissions may be achieved in 10% to 20% of patients with disease resistant to standard cisplatin-based regimens who are treated with high-dose carboplatin and etoposide with autologous bone marrow transplantation. The durable complete remission rate may exceed 50% if high-dose chemotherapy is used as salvage chemotherapy at the initial relapse of primary testicular cancer.
HOW TO DETECT THE PROGNOSIS OF TESTICULAR CARCINOMA?
The following factors affect prognosis (chance of recovery) of this cancer.
Stage of the cancer (whether it is in or near the testicle or has spread to other places in the body, and blood levels of AFP, β-hCG, and LDH).
Type of cancer.
Size of the tumor.
Number and size of retroperitoneal lymph nodes.
Testicular cancer is a highly treatable, often curable cancer. Some or all of the following factors may independently predict worse prognosis:
Presence of liver, bone, or brain metastases.
Very high serum markers.
Primary mediastinal nonseminoma.
Large number of lung metastases.
It is important to note that even patients with widespread metastases at presentation, including those with brain metastases, may still be curable and should be treated with this intent.
An important aspect of the follow-up of testicular cancer is the use of serum markers. Serum markers include AFP, HCG (measurement of the beta subunit reduces luteinizing hormone (LH) cross-reactivity), and lactate dehydrogenase (LDH). They may detect a tumor which is too small to be detected on physical examination or x-rays. Patients typically receive follow-up monthly for the first year and every other month for the second year after diagnosis and treatment. While the majority of tumor recurrences appear within 2 years, late relapse has been reported and lifelong marker, radiologic, and physical examination is recommended.
Patients who have been cured of testicular cancer have approximately a 2% to 5% cumulative risk of developing a cancer in the opposite testicle over the 25 years after initial diagnosis.
Good Prognosis
Nonseminoma:
Testis/retroperitoneal primary AND
No non-pulmonary visceral metastases AND
Good markers - all of:
AFP < 1000 ng/ml AND
hCG < 5000 iu/l (1000 ng/ml) AND
LDH < 1.5 x upper limit of normal
56% of nonseminomas
5-year progression-free survival (PFS) 89%; 5-year survival 92%
Seminoma:
Any primary site AND
No non-pulmonary visceral metastases AND
Normal AFP, any hCG, any LDH
90% of seminomas
5-year PFS 82%; 5-year survival 86%
Intermediate Prognosis
Nonseminoma:
Testis/retroperitoneal primary AND
No non-pulmonary visceral metastases AND
Intermediate markers - any of:
AFP >/= 1000 and hCG >/= 5000 iu/l and LDH >/= 1.5 x N* and 28% of nonseminomas
5-year PFS 75%; 5-year survival 80%
[Note: N indicates the upper limit of normal for the LDH assay.]
Seminoma:
Any primary site AND
Non-pulmonary visceral metastases AND
Normal AFP, any hCG, any LDH
10% of seminomas
5-year PFS 67%; 5-year survival 72%
Poor Prognosis
Nonseminoma:
Mediastinal primary OR
Non-pulmonary visceral metastases OR
For markers - any of:
AFP > 10,000 ng/ml OR
hCG > 50,000 iu/l (10,000 ng/ml) OR
LDH > 10 x upper limit of normal
16% of nonseminomas
5-year PFS 41%; 5-year survival 48%
Seminoma:
No patients classified as poor prognosis.
订阅：
博文 (Atom)
