卵巢癌、卵管癌和腹膜癌的FIGO分期(2014)
FIGO卵巢癌,输卵管癌
2012 FIGO 卵巢癌，输卵管癌1.1原发病灶：卵巢癌、输卵管癌和腹膜癌本章所用分期采用2006年FIGO分期。
目前，FIGO妇科肿瘤委员会正在修订卵巢癌、输卵管癌和原发性腹膜癌分期。
新分期需要相关领域的所有国际组织达成一致意见，2012年在罗马召开的FIGO大会中公布（实际上没有公布——译者注）。
如有可能，肿瘤的原发部位将被明确指出（如卵巢、输卵管或腹膜）。
某些情况下，可能无法确定肿瘤的原发位置，这种情况将列为“不明确的”[1,2]。
以前，我们常以为输卵管癌罕见[2]。
近年来病理学、分子学以及遗传学证据显示，许多被诊断为低分化浆液性卵巢癌和腹膜癌可能来源于输卵管伞端[3–8]。
因此，可能严重低估了输卵管癌的发病率。
当无法判断肿瘤原发部位时，以往通常认为肿瘤起源于卵巢，最新的研究结果支持将低分化浆液性卵巢癌、腹膜癌和输卵管癌看做一类疾病。
有建议采用更准确的术语“盆腔浆液性癌”（定义为肿瘤病理类型为浆液性且肿瘤源于卵巢、输卵管或腹膜）[9]。
目前尚无针对腹膜癌的分期，可参照FIGO分期标准；根据该标准不存在I 期腹膜癌。
1.1.1原发位置上皮性卵巢癌可来源于子宫内膜异位症或卵巢皮质包涵囊肿。
(卵巢癌二元论）它包括高分化子宫内膜样腺癌、透明细胞癌、交界性和高分化浆液性癌以及粘液性癌。
这类肿瘤可能由低级别前驱病变缓慢发展而来（内膜异位囊肿或囊腺瘤等），它们可归类为I类肿瘤[5]。
输卵管癌来源于输卵管远端，多数为低分化浆液性癌。
它们可由更隐蔽的前驱病变迅速发展而来，可归类为II类肿瘤[5,6]，这类疾病还包括低分化子宫内膜样腺癌和癌肉瘤，所有低分化恶性肿瘤都与TP53基因突变密切相关[5]。
（I型起病缓慢，II型起病迅速，侵袭能力强，高级别的卵巢浆液性癌起源于输卵管。
）1.1.2淋巴引流卵巢和输卵管的淋巴引流是通过子宫--卵巢骨盆漏斗韧带和圆韧带淋巴干和髂外的一分支引流到如下区域淋巴结：髂外、髂总、髂内、骶骨外侧和主动脉旁淋巴结，偶尔会引流入腹股沟淋巴结[1,10–12]。
第27章 卵巢肿瘤、输卵管肿瘤及原发性腹膜癌
妇产科学（第9版）
病理
侧别 质地 囊壁
囊内液 镜下
良性 多为单侧
浆液性肿瘤
交界性 双侧多见
单房或多房，囊性
多房囊性为主
单房：光滑， 多房：乳头（粗大， 不脆，以内生为主） 淡黄色浆液
乳头丰富，较细， 多数为外生性
浆液
单层立方或柱状上皮
①细胞轻、中度异型 ②复层上皮 ③无间质浸润
恶性 多为双侧 多房囊性，半实质性 大量乳头，分支细， 质脆，易脱落－恶性乳头
• 恶性肿瘤的鉴别诊断 – 子宫内膜异位症 – 盆腔结缔组织炎 – 结核性腹膜炎 – 生殖道以外的肿瘤
妇产科学（第9版）
治疗
卵巢肿瘤一经发现，应行手术。手术目的： ①明确诊断 ②切除肿瘤 ③恶性肿瘤进行手术病理分期 ④解除并发症
妇产科学（第9版）
治疗
• 术中应剖检肿瘤，必要时作冰冻切片组织学检查以明确诊 断
妇产科学（第9版）
组织学分类
• 分类方法多，最常用的是世界卫生组织的卵巢肿瘤组织 学分类（2014版)
分类 上皮性肿瘤
比例 50%～70%
生殖细胞肿瘤
20%～40%
性索-间质肿瘤 恶性转移性肿瘤
5%～8% 5%～10%
妇产科学（第9版）
组织学分类
一、上皮性肿瘤
1.浆液性肿瘤 2.黏液性肿瘤 3.子宫内膜样肿瘤 4.透明细胞肿瘤 5.移行细胞肿瘤 6.鳞状细胞肿瘤 7.混合性上皮性肿瘤 8.未分化和未分化类肿瘤
妇产科学（第9版）
恶性肿瘤随访
卵巢癌易于复发，需长期接受监测和随访。 随访时间：术后1年内，每3月随访1次；术后第2年后，每4-6个月 随访1次；第5年后每年1次。随访内容包括询问病史，体格检查 ，肿瘤标志物检测，影像学检查。CA125、AFP、HCG等肿瘤标志 物根据组织学类型选择。 超声检查异常再选择CT、MRT或PET-CT 检查。
卵巢癌、输卵管癌、腹膜癌手术分期标准-FIGO2014年
F I
G O2014年卵巢癌、输卵管癌、腹膜癌手术分期标准
注：（1）肿瘤原发部位——卵巢、输卵管还是腹膜应尽可能明确。
但是在某些情况下，可能无法确定肿瘤的原发位置，这种情况将列为“原发部位不明确”。
（2）应当记录肿瘤的组织学类型。
（3）新分期对Ⅲ期进行了修改，肿瘤扩散至腹膜后淋巴结但无腹腔内转移的
患者，分期被调整为ⅢA1期，这样调整的原因在于这些患者的预后显着优于发生腹腔内播散的患者。
（4）腹膜后淋巴结转移应当使用细胞学或组织学进行证实。
（5）肿瘤从大网膜扩散至脾或肝脏（ⅢC）应当与孤立性脾或肝实质转移相区别。
2024卵巢癌的基本介绍及病理分型
2024卵巢癌的基本介绍及病理分型在我国，卵巢癌年发病率居女性生殖系统肿瘤第3位，位于子宫颈癌和子宫体恶性肿瘤之后，呈逐年上升的趋势，而病死率位于女性生殖道恶性肿瘤之首。
卵巢恶性肿瘤包括多种病理类型，其中最常见的是上皮性癌，约占卵巢恶性肿瘤的80%,其次是恶性生殖细胞肿瘤和性索间质肿瘤，各约占10%和5%,本指南主要针对卵巢上皮性癌和恶性生殖细胞肿瘤。
卵巢深处盆腔，卵巢病变处于早期时常无特异临床症状，因出现症状就诊时，70%的患者已处于晚期。
卵巢癌具有一定的遗传性和家族聚集特征，目前已知与卵巢癌相关的遗传易感基因中以乳腺癌易感基因（BRCA影响最为显著。
BR约有20个，其CAl和BRCA2胚系突变携带者在一生之中发生卵巢癌的累积风险分别达54%和23%,是卵巢癌的高危人群。
对于BRCA1/2胚系突变携带者，推荐从30-35岁起开始定期行盆腔检查、血CA125和经阴道超声的联合筛查。
止匕外，还有林奇综合征、利-弗劳梅尼综合征家族的女性都是卵巢恶性肿瘤的高危人群，需要检测的基因还包括ATM、RAD51C x RAD51D、MLH1、MSH2、MSH6、PSM2、EPCAM x STK11等。
卵巢上皮癌多见于绝经后女性。
由于卵巢深居盆腔，卵巢上皮性癌早期症状不明显，往往是非特异性症状，难以早期诊断，约2/3的卵巢上皮性癌患者诊断时已是晚期。
晚期时主要因肿块增大或盆腹腔积液而出现相应症状，表现为下腹不适、腹胀、食欲下降等，部分患者表现为短期内腹围迅速增大，伴有乏力、消瘦等症状。
也可因肿块压迫出现大小便次数增多的症状。
出现胸腔积液者可有气短.难以平卧等表现。
卵巢恶性生殖细胞肿瘤常见于年轻女性，临床表现与上皮癌有所不同，早期即出现症状，除腹部包块腹胀外，常可因肿瘤内出血或坏死感染而出现发热，或因肿瘤扭转.肿瘤破裂等而出现急腹症的症状。
约60%~70%的患者就诊时属早期。
组织病理组织学检查是卵巢癌诊断的金标准。
卵巢癌分期
卵巢癌、卵管癌和腹膜癌的FIGO分期（2014）分享|发布时间：2014年06月04日点击数：3141 次字体：小大1973年FIGO首次发布卵巢癌、卵管癌和腹膜癌的分期，1988年有过一次修订。
本次为第三个版本。
卵巢癌不是一种单纯的疾病，包括数种临床和病理特点迥异的肿瘤。
大约90%为恶性上皮性癌（carcinomas）。
根据组织学、免疫组化和分子遗传学分析，至少有5种主要类型：高级别浆液性癌（70%），内膜样癌（10%），透明细胞癌（10%），粘液性癌（3%）和低级别浆液性癌（不足5%）。
上述类型占据约98%的卵巢癌类型。
恶性生殖细胞肿瘤（无性细胞瘤，卵黄囊瘤，未成熟畸胎瘤）约占3%，恶性潜能的性索间质肿瘤（主要是颗粒细胞瘤）约占1-2%。
原发性卵管癌和原发性腹膜癌比较罕见，和HGSC有很多相似的临床及形态特点，且主要发生在BRCA1/2遗传变异的女性中。
大量证据发现这些肿瘤主要为卵管起源。
而散发的HGSC则有多种来源可能。
既往“苗勒氏管新生化生（mullerian neometaplasia）”的概念得到更多证据支持。
而绝大部分ECs和CCCs则可能来源于内异症。
新的FIGO分期在2012年10月12日提交至FIGO执行委员会，2周后通过。
表1至表3是建议的具体分期系统。
准确的组织病理诊断对于卵巢癌成功分类及治疗至关重要，不同组织学类型对治疗的反应是不同的。
FIGO委员会选择的这种分类系统，将所有肿瘤类型共享的最相关的预后因素考虑在内。
但是，在诊断和分期的时候，仍应清楚说明具体卵巢癌的组织类型。
目前达成一致的组织学类型包括：1.上皮性癌（按频率顺序排列）：高级别浆液性癌（HGSC），内膜样癌（EC），透明细胞癌（CCC），粘液性癌（MC），低级别浆液性癌（LGSC）。
注：移行细胞癌目前认为是HGSC 的一种变异形态；恶性Brenner瘤则被认为是极端罕见的低级别癌。
2.恶性生殖细胞肿瘤（无性细胞瘤，卵黄囊瘤，未成熟畸胎瘤）。
卵巢癌病理figo分级i级
卵巢癌病理FIGO分级I级，指的是肿瘤局限在卵巢或输卵管内，没有或者很少有淋巴结转移。
根据FIGO（国际妇产科联盟）的定义，I级卵巢癌包括以下三个亚类：
1. IA类：肿瘤局限在单个卵巢或输卵管内，没有肿瘤破裂。
2. IB类：肿瘤局限在两个卵巢或输卵管内，没有肿瘤破裂。
3. IC类：肿瘤局限在一个或两个卵巢或输卵管内，有肿瘤破裂。
需要注意的是，FIGO分级只是对卵巢癌的病理严重程度进行了分类，具体的治疗方案还需要根据患者的个体情况（如年龄、身体状况等）和肿瘤的具体特征（如大小、生长速度、病理类型等）来制定。
妇科肿瘤PPT课件
其他CA125升高的常见原因
良性肿瘤和其他疾病 子宫内膜异位症 子宫肌瘤
PID OHSS 放疗 卵巢良性肿瘤
生理状态 月经来潮
妊娠 手术后
生物学特性
蛋白酶抑制剂家族 • 相应的底物和HE4的生物学功能未知 • 可能是抗菌、抗炎因子
HE4特点 • 在生殖系统和呼吸系统表达 • 卵巢癌最常见升高的标志物 • 无论疾病的早期还是晚期阶段，均出现mRNA和蛋白水平表达的升高 • 对 CA125有效补充
立因素 在肝癌、睾丸癌及一些良性肝脏疾病也可升高
参考范围<7ng/ml
其他原因： 恶性肿瘤 良性疾病或生理状态
原发性肝癌 病毒性肝炎、肝硬
化
卵巢生殖细胞肿瘤 妊娠
胃癌
胎儿神经管畸形
胰腺癌
双胎
结肠癌
CEA是应用最广泛是肿瘤标志物 在很多上皮性肿瘤，肺癌、乳腺癌、卵巢癌等都
有升高 也可在多种良性疾病中升高，胃肠道疾病、肺部
妇科肿瘤 与
肿瘤标志物
.
盆腔图
2014卵巢癌FIGO分期
I期：局限于卵巢
III期：局限于腹腔或腹膜后淋巴结
II期：局限于盆腔
IV期：远处转移
卵巢肿瘤组织来源
上皮性肿瘤：60% 生殖细胞肿瘤：30% 性索/间质肿瘤：8% 转移性肿瘤：2% 恶性肿瘤90%为上皮来源，高级别浆液
参考范围HE4 ＜140pmol/L
1 Bouchard D et al. Lancet Oncol 2006; 7, 167–74. 2 Hellström I et al. Cancer Res. 2003, 63, 3695–3700.
HE4 高表达
第18届FIGO世界妇产科学术会议纪要——卵巢肿瘤篇
仝国篡厦塑整董芒柱童盍２Ｑ塑至！堡旦蔓丝鲞蔓堕翅文章编号：１００５—２２１６（２００７）１０－０８０９—０３８０９ｔ医学动态第１８届ＦＩＧＯ世界妇产科学术会议纪要——卵巢肿瘤篇中图分类号：Ｒ７ｉ文献标志码：Ａ姚润斯。
罗新第１８届ＦＩＧＯ世界妇产科会议（ＸⅦＦＩＧＯＷｏｒｌｄＣｏｎ－ｇｒｅｓｓｏｆｃｙｎｅｃｏｌｏｇｙａｎｄＯｂｓｔｅ廿ｉｃｓ）于２００６年１１月５日至１０习在马来西亚的吉隆坡举行，来自世界各地的与会代表数千人。
在５天的会议期间，关于卵巢肿瘤方面的交流文章有７４篇，内容包括卵巢肿瘤的病因、病理、筛查、诊断、治疗、预后、特殊临床病例等方面。
ｌ发病高危因素及病因丹麦肿瘤流行病协会和肿瘤协会的研究表明，曾经妊娠、妊娠次数多、末次妊娠年龄较大、使用过口服避孕药和较长时间持续使用口服避孕药可以降低卵巢浆液性肿瘤、子宫内膜样肿瘤的发病风险．而吸烟是患黏液性卵巢癌的一个危险因素。
另一个研究用标准发病率比较不孕妇女与普通妇女患卵巢癌的风险，结果不孕妇女比普通妇女患卵巢癌的风险高，但需进一步证实究竟是激素治疗不孕症还是其他因素造成不孕症妇女的卵巢癌发病风险增高。
波兰医科大学介绍了类吗啡物质结合蛋自／细胞黏附分子（ＯＰＣＭＬ）近年来被认为可能是肿瘤抑制基因，ＯＰＣＭＬ基因在卵巢癌中的表达减少可能是由于启动子区的超甲基化使抑制因子功能丧失所致。
波兰Ｍｏｔｈｅｒ§Ｍｅｍｏｒｉａｌ医院和中国浙江大学的研究都发现，晚期卵巢癌妇女的外周血中ＣＤ４＋／ＣＤ２５＋调节Ｔ细胞增多而ＣＤ４／ＣＤ８Ｔ细胞的比侧下降，表明晚期卵巢癌妇女的免疫功能不良。
波兹南大学与预防和流行病学中心联合研究鉴定了卵巢癌或子宫内膜癌妇女中ＢＲＣＡＩ基因在１３位突变。
２１％的患者患卵巢癌。
波兰的多位学者还研究了外周血淋巴细胞与卵巢癌细胞问的相互作用。
结果示ＴＮＦ－ａｌｐｈａ和ＩＬ－２（Ｔｈｌ）水平下降，ＩＬ－１０和ＩＬ－６（Ｔｈ－２）生成增加。
2014年WHO卵巢肿瘤组织病理分类
粘液性交界性肿瘤/非典型增生性粘液性肿瘤
交界性
粘液性腺癌
恶性
子宫内膜样肿瘤
子宫内膜异位囊肿
良性
子宫内膜样囊腺瘤
良性
子宫内膜样腺纤维瘤
良性
子宫内膜样交界性肿瘤/非典型增生性子宫内膜样肿瘤
交界性
子宫内膜样腺癌
恶性
透明细胞肿瘤
透明细胞囊腺瘤
良性
透明细胞腺纤维瘤
良性
透明细胞交界性肿瘤/非典型增生性透明细胞肿瘤
非妊娠性绒癌
恶性
成熟性畸胎瘤
良性
未成熟畸胎瘤
恶性
混合性生殖细胞肿瘤
恶性
单胚层畸胎瘤和伴皮样囊肿的体细胞型肿瘤
良性卵巢甲状腺肿
良性
恶性卵巢甲状腺肿
恶性
类癌
恶性
卵巢甲状腺肿类癌
交界性
粘液性类癌
恶性
神经外胚层肿瘤
皮脂腺肿瘤
皮脂腺瘤
良性
皮脂腺癌
恶性
其他少见单胚层畸胎瘤
癌
鳞状细胞癌
恶性
其他
生殖细胞-性索间质肿瘤
成年型颗粒细胞瘤
恶性
幼年型颗粒细胞瘤
交界性
Sertoli细胞瘤
交界性
环状小管性索间质瘤
交界性
混合性性索间质肿瘤
Sertoli-Leydig细胞瘤
高分化型
良性
中分化型
交界性
伴异源成分
交界性
低分化型
恶性
伴异源成分
恶性
网状型
交界性
性索间质肿瘤(非特指)
交界性
生殖细胞肿瘤
无性细胞瘤
恶性
卵黄囊瘤
恶性
胚胎癌
2014FIGO外阴癌、宫颈癌和子宫内膜癌分期指南
FIGOGUIDELINESFIGO staging for carcinoma of the vulva,cervix,and corpus uteriFIGO Committee on Gynecologic Oncology 1International Journal of Gynecology and Obstetrics 125(2014)97–98Table 1Cancer of the vulva.FIGO StageDescription ITumor con fined to the vulva IALesions ≤2cm in size,con fined to the vulva or perineum and with stromal invasion ≤1.0mm a ,no nodal metastasis IBLesions N 2cm in size or with stromal invasion N 1.0mm a ,con fined to the vulva or perineum,with negative nodes IITumor of any size with extension to adjacent perineal structures (lower third of urethra,lower third of vagina,anus)with negative nodes IIITumor of any size with or without extension to adjacent perineal structures (lower third of urethra,lower third of vagina,anus)with positive inguinofemoral nodes IIIA(i)With 1lymph node metastasis (≥5mm),or (ii)With 1–2lymph node metastasis(es)(b 5mm)IIIB(i)With 2or more lymph node metastases (≥5m),or (ii)With 3or more lymph node metastases (b 5mm)IIICWith positive nodes with extracapsular spread.IVTumor invades other regional (upper 2/3urethra,upper 2/3vagina),or distant structures IVA Tumor invades any of the following:(i)upper urethral and/or vaginal mucosa,bladder mucosa,rectal mucosa,or fixed to pelvic bone,or(ii)fixed or ulcerated inguinofemoral lymph nodesIVBAny distant metastasis including pelvic lymph nodes a The depth of invasion is de fined as the measurement of the tumor from the epithelial –stromal junction of the adjacent most super ficial dermal papilla to the deepest point of invasion.Table 2Cancer of the cervix uteri.StageDescription IThe carcinoma is strictly con fined to the cervix (extension to the uterine corpus should be disregarded).IA Invasive cancer identi fied only microscopically.(All gross lesions even with super ficial invasion are Stage IB cancers.)Invasion is limited to measured stromal invasionwith a maximum depth of 5mm a and no wider than 7mm.IA1Measured invasion of stroma ≤3mm in depth and ≤7mm width.IA2Measured invasion of stroma N 3mm and b 5mm in depth and ≤7mm width.IB Clinical lesions con fined to the cervix,or preclinical lesions greater than stage IA.IB1Clinical lesions no greater than 4cm in size.IB2Clinical lesions N 4cm in size.II The carcinoma extends beyond the uterus,but has not extended onto the pelvic wall or to the lower third of vagina.IIA Involvement of up to the upper 2/3of the vagina.No obvious parametrial involvement.IIA1Clinically visible lesion ≤4cmIIA2Clinically visible lesion N 4cmIIB Obvious parametrial involvement but not onto the pelvic sidewall.III The carcinoma has extended onto the pelvic sidewall.On rectal examination,there is no cancer free space between the tumor and pelvic sidewall.The tumor involvesthe lower third of the vagina.All cases of hydronephrosis or non-functioning kidney should be included unless they are known to be due to other causes.IIIA Involvement of the lower vagina but no extension onto pelvic sidewall.IIIB Extension onto the pelvic sidewall,or hydronephrosis/non-functioning kidney.IV The carcinoma has extended beyond the true pelvis or has clinically involved the mucosa of the bladder and/or rectum.IVA Spread to adjacent pelvic organs.IVB Spread to distant organs.aThe depth of invasion should not be more than 5mm taken from the base of the epithelium,either surface of glandular,from which it originates.Vascular space invasion should not alter the staging.1Committee members:H.Belhadj (Switzerland),J.Berek (USA),A.Bermudez (Argentina),N.Bhatla (India),J.Cain (USA),L.Denny (Chair;South Africa),K.Fujiwara (Japan),N.Hacker (Australia),E.Åvall-Lundqvist (Sweden),D.Mutch (USA),F.Odicino (Italy),S.Pecorelli (Italy),J.Prat (Spain),M.Quinn (Co-chair;Australia),M.A-F.Seoud (Lebanon),S.K.Shrivastava (India)./10.1016/j.ijgo.2014.02.0030020-7292/©2014Published by Elsevier Ireland Ltd.on behalf of International Federation of Gynecology andObstetrics.Contents lists available at ScienceDirectInternational Journal of Gynecology and Obstetricsj o u r n a l h o m e p a g e :w w w.e l s e vi e r.c o m/l o c a t e /i j g o98International Journal of Gynecology and Obstetrics125(2014)97–98Table3Cancer of the corpus uteri.FIGO StageI a Tumor confined to the corpus uteriIA a No or less than half myometrial invasionIB a Invasion equal to or more than half of the myometriumII a Tumor invades cervical stroma,but does not extend beyond the uterus bIII a Local and/or regional spread of the tumorIIIA a Tumor invades the serosa of the corpus uteri and/or adnexae cIIIB a Vaginal involvement and/or parametrial involvement cIIIC a Metastases to pelvic and/or para-aortic lymph nodes cIIIC1a Positive pelvic nodesIIIC2a Positive para-aortic nodes with or without positive pelvic lymph nodesIV a Tumor invades bladder and/or bowel mucosa,and/or distant metastasesIVA a Tumor invasion of bladder and/or bowel mucosaIVB a Distant metastasis,including intra-abdominal metastases and/or inguinal nodes)a Either G1,G2,or G3.b Endocervical glandular involvement only should be considered as Stage I and no longer as Stage II.c Positive cytology has to be reported separately without changing the stage.。
FIGO2021妇癌报告：卵巢癌、输卵管癌、腹膜癌诊治指南解读(全文)
FIGO2021妇癌报告：卵巢癌、输卵管癌、腹膜癌诊治指南解读（全文）卵巢癌的三种类型一、概述卵巢恶性肿瘤可以发生于任何年龄。
20岁以下女性中生殖细胞肿瘤最常 见。
交界性W 瘤常好发于30余岁到40余岁的女性，发病年龄较上皮性浸 润癌患者早10岁以上。
卵巢上皮性癌绝大多数发生于50岁以后。
卵巢上皮性癌较确定的致病危险因素为生育因素。
未生育女性罹患卵巢上皮性癌的风险是已生育女性的2倍。
以往认为输卵管癌罕见，但已有证据显示,不少高级别浆液性卵巢癌和腹 膜癌源于输卵管伞端。
二、组织学分类特异性性索间质细胞肿瘤约10%上皮性肿瘤约为 卵巣癌的50%~70% 生殖细胞 瘤约10%大多数卵巢癌为上皮来源，国际妇产科联盟(FIGO )采用世界卫生组织(WHO )卵巢上皮性癌组织学分类方法。
分为：(1 )浆液性肿瘤。
(2 )黏液性肿瘤。
(3 )内膜样肿瘤。
(4 )透明细胞肿瘤。
(5 )伯纳勒肿瘤。
(6)未分化癌(属于恶性上皮结构肿瘤，但它们分化极差，无法分入任何一组)。
(7 )混合型上皮性«瘤(肿瘤由5种常见上皮性肿瘤中的2种或以上组成,具体种类通常会明确说明)。
(8)腹膜癌或原发部位不明确的浆液性癌：病理为高级别浆液性癌，外观上卵巢和输卵管被附带累及且它们并非原发部位。
其中浆液性癌是最常见的类型。
90%以上输卵管癌是浆液性癌或高级别子宫内膜癌。
三、遗传学约20%卵巢癌、输卵管癌和腹膜癌与遗传因素有关：(1 )多数遗传性卵巢癌是BRCA1或BRCA2发生有害突变导致的。
在非黏液性高级别卵巢癌患者中,至少15%存在胚系BRCA1/2突变,这些患者中40%没有乳腺癌/卵巢癌家族史。
推荐所有非黏液性高级别卵巢癌患者都应接受基因检测，即便她们没有乳腺癌/卵巢癌家族史。
(2 )BRCA1和BRCA2遗传性有害突变是最主要的遗传风险因素O BRCA1 突变携带者癌变的发生率为20%~50% ,而BRCA2突变携带者癌变发生率为10%~20%。
卵巢癌、卵管癌和腹膜癌的FIGO分期(2014)
ClinicalCommentary2014FIGO staging for ovarian,fallopian tube and peritoneal cancerCancer staging is a core principle in understanding the severity of pa-tients'clinical condition,predicting the outcome,and planning ade-quate treatment.Staging is necessary for explaining epidemiologic changes,de fining the disease at presentation,and evaluating the overall impact of new therapies.In essence,it assigns patients to prognostic groups that require speci fic treatments.The steps of staging typically begin by establishing the histopathologic diagnosis,according to the tumor cell type,and assessing prognosis based on extent of disease and other known prognostic parameters.Recently,the presence of var-ious molecular genetic alterations has been used in the establishment of prognosis and even staging classi fication in some tumors but gyneco-logic cancers have continued to rely on physical,radiographic and surgi-cal findings.This editorial is written to make the readership aware of the recent changes that have been made by the International Federation of Gyne-cology and Obstetrics (FIGO)in the staging classi fication of ovarian can-cer and the reasoning behind those changes [1].Even if the FIGO Committee on Gynecologic Oncology utilized the best evidence current-ly available,this is always a somewhat subjective process.Furthermore,one needs to be aware that FIGO is an international organization that must take into account the needs of women with gynecologic cancers throughout the world,and not just those from countries that are re-source rich.The first FIGO ovarian cancer staging was published in 1973in Volume 15of the FIGO Annual Report.Since that time there have been two other changes including this one in 1988and 2013.Ovarian cancer is not one disease.Several distinct tumors with unique clinical and pathological features may arise in the ovary.Approx-imately 90%of ovarian cancers are carcinomas (malignant epithelial tu-mors)and,based on histopathology,immunohistochemistry,and molecular genetic analysis,at least 5main types are currently distin-guished:high-grade serous carcinoma (HGSC [70%]);endometrioid car-cinoma (EC [10%]);clear-cell carcinoma (CCC [10%]);mucinous carcinoma (MC [3%]);and low-grade serous carcinoma (LGSC [less than 5%][2]).These tumor types (which account for 98%of ovarian car-cinomas)can be reproducibly diagnosed by light microscopy and are es-sentially different diseases,as indicated by differences in epidemiologic and genetic risk factors;precursor lesions;ways of spread;and molecu-lar changes during oncogenesis,response to chemotherapy,and out-come [3]Much less frequent are malignant germ cell tumors (dysgerminomas,yolk sac tumors,and immature teratomas [3%of ovar-ian cancers])and potentially malignant sex cord-stromal tumors (1%–2%,mainly granulosa cell tumors).The biomarker expression pro file within a given histotype is consistent across stages.In short,ovarian cancers differ primarily based on histotype.Primary fallopian tube cancer and primary peritoneal cancer are rare malignancies but share many clinical and morphologic similarities with HGSC;i.e.,the most common type of ovarian cancer (in the past,re-ferred to as “papillary serous carcinoma ”)and the prototype tumor oc-curring in women with BRCA1or BRCA2germline mutations.In these patients,compelling evidence for a tubal derivation of their tumors,mainly those encountered at early stage,has accumulated over the past decade [4–6].Evidence of a tubal origin is weaker in the far more common sporadic HGSCs,and a multicentric origin of these tumors (i.e.arising from ovarian surface mesothelial invaginations or cortical inclusion cysts,implantation of tubal-type epithelium into the ovary [endosalpingiosis],or the pelvic peritoneum [the so-called secondary müllerian system ])cannot be ruled out.Recently,it has been hypothe-sized that cytokeratin7-positive embryonic/stem cells would be capable of mullerian differentiation in cortical inclusion cysts resulting from ovarian surface epithelium (mesothelium)invaginations.Thus,embry-onic progenitors would give rise to immunophenotypically distinct neo-plastic progeny [7]which would support the old concept of “mullerian neometaplasia ”.On the other hand,it has been demonstrated that the vast majority of ECs and CCCs arise in the ovary from endometriosis.Based on the putative tubal or peritoneal origin of a number of BRCA +HGSCs,and the fact that they are managed clinically in a similar manner regardless their ovarian,tubal,or peritoneal derivation,most FIGO Committee members felt that FIGO staging of ovarian,peritoneal,and fallopian tube cancers should be considered collectively [8].The pri-mary site (i.e.ovary,fallopian tube,or peritoneum)should be designat-ed where possible.In some cases,it might not be possible to delineate the primary site clearly;such cases should be listed as “undesignated.”The process of updating the staging classi fication of ovarian,fallopian tube,and primary peritoneal cancer started 4years ago with a proposal that was sent to all relevant gynecology oncology organiza-tions and societies throughout the world and input was collated,evalu-ated,and formulated into the staging that is presented below.All suggestions are based on the best available evidence.The committee ac-knowledged that there are areas that are not supported by strong evi-dence and has been careful to ensure that changes are not made without quality evidence when available.The new staging below was reached by consensus of all participating in the FIGO meeting held in Rome,Italy,on October 7th,2012,some of whom were representatives of their organizations.The new staging was presented to the FIGO Exec-utive Board on October 12,2012,and approved two weeks later.Ovarian cancer remains largely a surgically staged disease.The prog-nosis is based on histologic type,radiographic,and operative extent of the disease.The proposed staging system is noted below (Table 1).(See Tables 2and 3).Precise histopathologic diagnosis is mandatory for successful catego-rization and treatment of ovarian cancers,as different histologic types respond differently to treatment.To be practical,the FIGO committeeGynecologic Oncology 133(2014)401–404/10.1016/j.ygyno.2014.04.0130090-8258/©2014Elsevier Inc.All rightsreserved.Contents lists available at ScienceDirectGynecologic Oncologyj o u r na l h om e p a g e :w w w.e l s e v i e r.c o m /l o c a t e /y g y n ochose a staging classi fication system that takes into account the mostrelevant prognostic parameters shared by all tumor types.However,it was agreed on by all that histologic type should be designated at the time of diagnosis and staging.The five agreed upon epithelial histologic types,as well as much less common malignant germ cell and potentially malignant sex cord-stromal tumors,are listed below.Histologic types:Carcinomas (by order of frequency)High-grade serous carcinoma (HGSC)Endometrioid carcinoma (EC)Clear-cell carcinoma (CCC)Mucinous carcinoma (MC)Low-grade serous carcinoma (LGSC).Note:Transitional cell carcinoma is currently interpreted as a mor-phologic variant of HGSC;malignant Brenner tumor is considered a low-grade carcinoma which is extremely rare.Malignant germ cell tumors (dysgerminomas,yolk sac tumors,and immature teratomas)Potentially malignant sex cord-stromal tumors (mainly rare cases of granulosa cell tumors and Sertoli –Leydig cell tu-mors with heterologous sarcomatous elements).The issues discussed and concluded by the FIGO committee will be taken one stage at a time,controversial issues raised,and the available data cited as appropriate.Staging should be considered fluid.As more prognostic features be-come available these should be used to further predict outcomes and determine treatment.The world is getting smaller in the sense that staging systems must be applicable universally and including resource rich as well as resource poor regions.Toward this end,three members of FIGO will now be on the AJCC staging committee and there is repre-sentation of the UICC on the AJCC.The International Gynecologic Cancer Society and the Society of Gynecologic Oncology now have nonvoting representation on the FIGO committee as well.We need to continue to gain consensus internationally by having cross representation on ourTable 12014FIGO ovarian,fallopian tube,and peritoneal cancer staging system and corresponding TNM.I Tumor con fined to ovaries or fallopian tube(s)T1IA Tumor limited to one ovary (capsule intact)or fallopian tube,No tumor on ovarian or fallopian tube surface No malignant cells in the ascites or peritoneal washingsT1a IBTumor limited to both ovaries (capsules intact)or fallopian tubesNo tumor on ovarian or fallopian tube surfaceNo malignant cells in the ascites or peritoneal washingsT1b ICTumor limited to one or both ovaries or fallopian tubes,with any of the following:IC1Surgical spill intraoperativelyIC2Capsule ruptured before surgery or tumor on ovarian or fallopian tube surface IC3Malignant cells present in the ascites or peritoneal washingsT1c II Tumor involves one or both ovaries or fallopian tubes with pelvic extension (below pelvic brim)or peritoneal cancer (Tp)T2IIA Extension and/or implants on the uterus and/or fallopian tubes/and/or ovaries T2a IIB Extension to other pelvic intraperitoneal tissuesT2bIIITumor involves one or both ovaries,or fallopian tubes,or primary peritoneal cancer,with cytologically or histologically con firmed spread to the peritoneum outside the pelvis and/or metastasis to the retroperitoneal lymph nodesT3IIIA Metastasis to the retroperitoneal lymph nodes with or without microscopic peritoneal involvement beyond the pelvis T1,T2,T3aN1IIIA1Positive retroperitoneal lymph nodes only (cytologically or histologically proven)IIIA1(i)Metastasis ≤10mm in greatest dimension (note this is tumor dimension and not lymph node dimension)T3a/T3aN1IIIA1(ii)Metastasis N 10mm in greatest dimension IIIA 2Microscopic extrapelvic (above the pelvic brim)peritoneal involvement with or without positive retroperitoneal lymph nodes T3a/T3aN1IIIB Macroscopic peritoneal metastases beyond the pelvic brim ≤2cm in greatest dimension,with or without metastasis to the retroperitoneal lymph nodes T3b/T3bN1III C Macroscopic peritoneal metastases beyond the pelvic brim N 2cm in greatest dimension,with or without metastases to the retroperitoneal nodes (Note 1)T3c/T3cN1IVDistant metastasis excluding peritoneal metastasesStage IV A:Pleural effusion with positive cytologyStage IV B:Metastases to extra-abdominal organs (including inguinal lymph nodes and lymph nodes outside of abdominal cavity)(Note 2)Any T,Any N,M1(Note 1:includes extension of tumor to capsule of liver and spleen without parenchymal involvement of either organ)(Note 2:Parenchymal metastases are Stage IV B)T3c/T3cN1)Notes:1.Includes extension of tumor to capsule of liver and spleen without parenchymal involvement of either organ.2.Parenchymal metastases are Stage IV B.Table 2Carcinoma of the ovary –fallopian tube –peritoneum —stage grouping.FIGOUICC(Designate primary:Tov,Tft,Tp or Tx)Stage T N M IA T1a N0M0IB T1b N0M0IC T1c N0M0IIA T2a N0M0IIB T2b N0M0IIIA T3a N0M0T3a N1M0IIIB T3b N0M0T3b N1M0IIIC T3c N0–1M0T3c N1M0IV Any T Any N M1Regional nodes (N)Nx Regional lymph nodes cannot be assessed N0No regional lymph node metastasis N1Regional lymph node metastasis Distant metastasis (M)Mx Distant metastasis cannot be assessed M0No distant metastasis M1Distant metastasis (excluding peritoneal metastasis)Notes:1.The primary site –i.e.ovary,fallopian tube or peritoneum –should be designated where possible.In some cases,it may not be possible to clearly delineate the primary site,and these should be listed as ‘undesignated ’.2.The histologic type of should be recorded.3.The staging includes a revision of the stage III patients and allotment to stage IIIA1is based on spread to the retroperitoneal lymph nodes without intraperitoneal dissemina-tion,because an analysis of these patients indicates that their survival is signi ficantly bet-ter than those who have intraperitoneal dissemination.4.Involvement of retroperitoneal lymph nodes must be proven cytologically or histologically.5.Extension of tumor from omentum to spleen or liver (Stage III C)should be differentiat-ed from isolated parenchymal splenic or liver metastases (Stage IVB).402Clinical Commentaryentire representative staging committees.This will help us standardize care and staging systems throughout the world.In the future it is hoped that organizations such as UICC,AJCC,and FIGO will continue to work together to achieve this goal.Conflict of interest statementThe authors declare that there are no conflicts of interest.References[1]Prat J.Staging classification for cancer of the ovary,fallopian tube,and peritoneum.Int J Gynecol Obstet2014;124:1–5.[2]Lee KR,Tavassoli FA,Prat J,Dietel M,Gersell DJ,Karseladze AI,et al.Surface epithelialstromal tumours:tumours of the ovary and peritoneum.In:Tavassoli FA,Devilee P,ed-itors.World Health Organization Classification of Tumours:pathology and genetics of tumours of the breast and female genital organs.Lyon:IARC Press;2003.p.117–45.[3]Prat J.Ovarian carcinomas:five distinct diseases with different origins,genetic alter-ations,and clinicopathological features.Virchows Arch2012;460(3):237–49.[4]Piek JM,van Diest PJ,Zweemer RP,Jansen JW,Poort-Keesom RJ,Menko FH,et al.Dysplastic changes in prophylactically removed Fallopian tubes of women predisposed to developing ovarian cancer.J Pathol2001;195(4):451–6.[5]Callahan MJ,Crum CP,Medeiros F,Kindelberger DW,Elvin JA,Garber JE,et al.Prima-ry fallopian tube malignancies in BRCA-positive women undergoing surgery for ovarian cancer risk reduction.J Clin Oncol2007;25(25):3985–90.[6]Kindelberger DW,Lee Y,Miron A,Hirsch MS,Feltmate C,Medeiros F,et al.Intraepithelial carcinoma of thefimbria and pelvic serous carcinoma:Evidence fora causal relationship.Am J Surg Pathol2007;31(2):161–9.[7]Crum CP,Herfs M,Ning G,Bijron JG,Howitt BE,Jimenez CA,Hanamornroongruang S,McKeon FD,Xian W.Through the glass darkly:intraepithelial neoplasia,top-down differentiation,and the road to ovarian cancer.J Pathol2013;231(4):402–12. [8]Cannistra SA,Gershenson DM,Recht A.Ovarian cancer,fallopian tube carcinoma,and peritoneal carcinoma.In:De Vita VT,Lawrence TS,Rosenberg SA,editors.De Vita,Hellman,and Rosenberg's cancer:principles and practice of oncology.9th ed.Philadelphia:Lippincott,Williams,Wilkins;2011.p.1368–91.[9]Yemelyanova AV,Cosin JA,Bidus MA,Boice CR,Seidman JD.Pathology of stage I ver-sus stage III ovarian carcinoma with implications for pathogenesis and screening.Int J Gynecol Cancer2008;18(3):465–9.[10]Seidman JD,Yemelyanova AV,Khedmati F,Bidus MA,Dainty L,Boice CR,et al.Prog-nostic factors for stage I ovarian carcinoma.Int J Gynecol Pathol2010;29(1):1–7.Table3Explantation of the Staging ChangesStage IDisease confined to the ovary after comprehensive staging T1–N0–M0 Stages IA and IB are unchanged from the1988staging.T1a–N0–M0 IA remains tumor limited to one ovary(capsule intact)or fallopian tube.There can be no disease on the ovary or fallopian tube surface.There are no malignant cells inthe ascites or peritoneal washings.Primary peritoneal has no Stage IA.1B is unchanged and remains tumor limited to both ovaries with capsule intact or fallopian tubes;and there can be no malignant cells on ovarian or fallopian tubesurfaces.There are no malignant cells in the ascites or peritoneal washings.T1b–N0–M0 IC represents a change for the1988staging system.It still designates positive cytology but,if possible,must designate the reason for malignant cells being present;hence,this substage is divided into three groups.T1c–N0–M01C1represents disease confined to one or both ovaries with capsule rupture during surgery1C2represents rupture before surgery or tumor excrescences on the surface of the tube or ovary.1C3represents malignant cells in the peritoneal cavity regardless of cause.CommentsSpecific issues surrounding stage I tumors need to be considered when evaluating Stage I patients surgically and pathologically.Bilateral tumors that are large on oneside and multiple or small on the other could represent metastases up to one third of the time[9,10].The significance of positive cytology is poorly understood andis one of the reasons that the committee elected to divide it into three categories.Some studies have found that intraoperative rupture portends a worse prognosisthan if the capsule is unruptured.In one multivariate analysis,both capsule rupture and positive cytology were independent predictors of worse disease freesurvival[11].Surface involvement of the ovary or fallopian tube should be considered present only when excrescences have cancer cells in direct contact with theperitoneal cavity,breaking through the surface of the ovarian capsule.Tumors with a smooth surface usually don't show an exposed layer of neoplastic cells.Histologic grade influences survival and is given with the histotype except for endometrioid carcinoma and mucinous cancers which should be graded.Practicallyall clear cell carcinomas are high grade.Stage IIStage II ovarian cancer includes disease confined to the pelvis(below the pelvic brim).It involves one or both ovaries or fallopian tubes with pelvic extension orprimary peritoneal cancer.T2–N0–M0IIA Extension and/or implants on the uterus and/or fallopian tubes and/or ovaries T2a–N0–M0 IIB Extension to other pelvic intraperitoneal tissues/organs T2b–N0–M0 Comments:Stage II ovarian cancer remains controversial and ill defined.It comprises a small group of ovarian cancer patients that have direct extension of their tumors to otherpelvic organs without evidence of metastatic disease.However,it also includes a group of patients that has metastases to the pelvic peritoneum.In this secondgroup of patients,disease is similar to that of stage III patients.Disease invading through the bowel wall and into the mucosa increases the stage to IVB.Stage IIIStage III Cancer involves1or both ovaries,fallopian tubes,or is primarily from the peritoneum with histologically confirmed spread outside of the pelvis and/ormetastases to the retroperitoneal nodes.T1/T2–N1–MO IIIA1Positive retroperitoneal nodes only.This can be confirmed histologically or cytologically.lllA(i)Metastases up to and including10mm in greatest dimensionIIIA(ii)Metastases more than10mm in greatest dimensionStage IIIA2:Microscopic extrapelvic(above the boney pelvic brim)peritoneal involvement with or without metastases to the retroperitoneal lymph nodes T3a2–N0/N1–M0IIIB:Macroscopic peritoneal metastases beyond the pelvis up to and including2cm in greatest dimension,with or without metastases to the retroperitoneal lymph nodes.T3b–N0/N1–M0IIIC:Macroscopic peritoneal disease beyond the pelvis more than2cm in greatest diameter,with or without metastases to the retroperitoneal lymph nodes(includes tumor extension to the capsule of the liver and spleen but no parenchymal metastases).CommentsApproximately,85%of ovarian cancers present as stage III tumors and the vast majority are high-grade serous carcinomas[12].A little less than10%of patients with ovarian cancer that appear to have stage I disease will have isolated lymph node metastases.The likelihood of having nodal metastasis in other stages are:III,55% and IV,88%[13].There is some evidence that exclusive retroperitoneal disease portends a better prognosis and for this reason the new staging system addresses this issue in the IIIA category[14–19].It should be noted that the size separating the IIIA tumors applies to the tumor size and not the lymph node size.Stage IV:Distant metastases excluding peritoneal or retroperitoneal nodal disease below the diaphragm.IVA:Pleural effusion with positive cytologyIVB:Metastases to extra abdominal sites including inguinal lymph nodes and parenchymal involvement of visceral organs including liver and spleen.Transmural involvement of a visceral structure also represents stage IVB disease.403Clinical Commentary[11]Bakkum-Gamez JN,Richardson DL,Seamon LG,Aletti GD,Powless CA,Keeney GL,et al.Influence of intraoperative capsule rupture on outcomes in stage I epithelial ovarian cancer.Obstet Gynecol2009;113(1):11–7.[12]Heintz AP,Odicino F,Maisonneuve P,Quinn MA,Benedet JL,Creasman WT,et al.Carcinoma of the ovary.FIGO26th annual report on the results of treatment in gy-necologic cancer.Int J Gynecol Obstet2006(95Suppl.1):S161-92.[13]Ayhan A,Gultekin M,Dursun P,Dogan NU,Aksan G,Guven S,et al.Metastaticlymphnode number in epithelial ovarian carcinoma:does it have any clinical signif-icance?Gynecol Oncol2008;108(2):428–32.[14]Onda T,Yokishikawa H,Yasugi T,Mishima M,Nakagawa S,Yamada M,et al.Patientswith ovarian carcinoma upstaged to stage III after systemic lymphadenectomy have similar survival to Stage I/II patients and superior survival to other stage III patients.Cancer1998;83(8):1555–60.[15]Kanazawa K,Suzuki T,Tokashika M.The validity and significance of substage IIIC bynode involvement in ovarian cancer:impact of nodal metastasis on patient survival.Gynecol Oncol1999;73(2):237–41.[16]Panici PB,Maggioni A,Hacker N,Landoni F,Ackerman S,Campagnutta E,et al.Sys-tematic aortic and pelvic lymphadenectomy versus resection of bulky nodes only in optimally debulked advanced ovarian cancer:a randomized clinical trial.J Natl Can-cer Inst2005;97(8):560–6.[17]Cliby WA,Aletti GD,Wilson TO,Podratz KC.Is it justified to classify patients to stageIIIC epithelial ovarian cancer based on nodal involvement only?Gynecol Oncol 2006;103(3):797–801.[18]Ferrandina G,Scambia G,Legge F,Petrillo M,Salutari V.Ovarian cancer patients with“node positive-only”Stage IIIC disease have a more favorable outcome than Sage IIIA/B.Gynecol Oncol2007;107(1):154–6.[19]Baek SJ,Park JY,Kim DY,Kim JH,Kim YM,Kim YT,et al.Stage IIIC epithelial ovariancancer classified soley by lymph node metastasis has a more favorable prognosis than other types of stage IIIC epithelial ovarian cancer.J Gynecol Oncol 2008;19(4):223–8.David G.Mutch Department of Obstetrics and Gynecology,Washington University School of Medicine,4911Barnes Hospital Plaza,St.Louis,MO63110,United StatesJaime Prat Department of Pathology,Hospital de la Santa Creu i Sant Pau,Autonomous University of Barcelona,Sant Quinti,87-89,08041Barcelona,Spain404Clinical Commentary。
第九版妇产科学配套课件 27 卵巢肿瘤、输卵管肿瘤及原发性腹膜癌
临床表现
良性肿瘤 • 生长缓慢，早期无症状 • 增大后感腹胀不适，可扪及肿块 • 压迫症状：尿频、便秘等 • 体征：
➢ 妇检可及盆腔包块 ➢ 囊性或实质性 ➢ 光滑，无粘连，活动好
恶性肿瘤 • 早期多无症状，出现症状时已属晚期：
腹胀、腹部肿块和腹腔积液 • 晚期：疼痛，下肢浮肿，恶病质等 • 体征：
ⅠC2 手术前包膜已破裂或卵巢、输卵管表面有肿瘤
ⅠC3 腹腔积液或腹腔冲洗液发现癌细胞
Ⅱ期 ⅡA ⅡB
肿瘤累及单侧或双侧卵巢并有盆腔内扩散（在骨盆入口平面以下）或原发性腹膜癌 肿瘤蔓延或种植到子宫和（或）输卵管和（或）卵巢 肿瘤蔓延至其他盆腔内组织
卵巢癌、输卵管癌、原发性腹膜癌的手术-病理分期（FIGO，2014年）（续表
诊断
结合病史和体征，辅以必要的辅助检查确定： • 肿块是否来自卵巢 • 肿块的性质是否为肿瘤 • 肿块是良性还是恶性 • 可能组织学类型 • 恶性肿瘤的转移范围
早期诊断是降低卵巢癌死亡率主要措施之一，目前 各种诊断方法尚不能达到此目的
影像学检查 • B型超声检查：可了解肿块的部位、大小、形态，囊性或实性，囊内有无乳
--孙思邈
第27章 卵巢肿瘤、输卵管肿瘤 及原发性腹膜癌
授课人：XX XX
目录
第一节 卵巢肿瘤概论 第二节 卵巢上皮性肿瘤 第三节 卵巢非上皮性肿瘤 第四节 卵巢转移性肿瘤
重点难点
掌握 掌握各类卵巢肿瘤的临床表现、并发症、诊断、鉴别诊断和 初次治疗原则。
熟悉 熟悉卵巢肿瘤的组织学分类、主要组织学类型的病理特征和 恶性肿瘤的转移途径。
头，临床诊断符合率>90%；彩色多普勒超声扫描可测定肿块血流变化，有 助于诊断。 • MRI、CT检查：MRI可较好显示肿块及肿块与周围的关系，有利于病灶定 位及病灶与相邻结构关系的确定；CT可判断周围侵犯及远处转移情况，对 手术方案的制定有较大优势。
卵巢癌FIGO分期与C反应蛋白相关性分析
卵巢癌FIGO分期与C反应蛋白相关性分析目的：探讨卵巢癌病理分期与术前C反应蛋白值的相关性。
方法：回顾性分析2008年1月-2012年6月手术的98例初治卵巢癌患者的病理资料及术前C 反应蛋白值，并与同期手术的60例卵巢良性肿瘤进行比较分析。
结果：早期组平均C反应蛋白值为（6.65±3.56）mg/L，晚期组为（43.70±23.85）mg/L，对照组为（3.13±0.55）mg/L，早期组与晚期组与对照组在C反应蛋白值上比较差异均有统计学意义（P＜0.05），晚期组C反应蛋白升高比例（75%）显著高于早期组（23.5%），比较差异有统计学意义（P＜0.05）。
结论：C反应蛋白与卵巢癌病理分期密切相关，C反应蛋白对于卵巢肿瘤性质鉴别及病理分期预测有重要价值，从而对疾病预后有一定意义。
[Abstract] Objective：To investigate the relationship between staging of ovarian cancer with C-reactive protein.Method：The case of 98 ovarian cancer patients were selected from January 2008 to June 2012，and clinicopathological and C-reactive protein data were analyzed retrospectively.Result：The mean C-reactive protein was （6.65±3.56）mg/L in the early stage ovarian cancer group，（43.70±23.85）mg/L in the advanced stage ovarian cancer group，and （3.13±0.55）mg/L in the control pared with the control group，there were significant differences in the data of C-reactive protein in patients with ovarian cancer.The same results were also observed between advanced groups and early groups（P＜0.05）.Conclusion：CRP is closely related to the pathologic staging of ovarian cancer，CRP is important for the identification of benign and malignant ovarian tumor diagnosis and the prediction of pathological staging，which have certain significance to the prognosis of ovarian carcinaoma.[Key words] Ovarian cancer；Pathological staging；C-reactive protein卵巢癌是女性常见恶性肿瘤，起病隐匿，多数患者就诊时已属晚期（Ⅲ～Ⅳ期），病死率高，居妇科恶性肿瘤首位。
卵巢癌诊疗规范
卵巢癌诊疗规范一、概述上皮性卵巢癌、输卵管癌及原发性腹膜癌（以下简称“卵巢癌”）在全球女性生殖系统恶性肿瘤中发病率位列第3，死亡率位列第2。
我国每年卵巢癌新发病例 5.21万人，死亡病例 2.25万人，是威胁女性健康的重要疾病之一。
卵巢癌起病隐匿且缺乏有效的筛查手段，多数患者直到出现盆腔包块、腹水、远处转移才被发现。
确诊时，约三分之二患者已存在腹盆腔内的肿瘤播散。
卵巢癌总体治疗效果并不理想，约80%的患者在初始治疗后最终复发，中位复发时间仅 16个月。
因此，规范化诊治尤为重要。
二、FIGO 分期2014 年国际妇科肿瘤联盟（FIGO）更新了相应分期，主要有以下变化：①将 IC 期详细分为3 类，IC1 术中肿瘤破裂；IC2 术前肿瘤破裂或肿瘤位于卵巢/输卵管表面；IC3 腹腔冲洗液或腹水阳性。
②取消ⅡC 期（局限在真骨盆的一侧或双侧卵巢/输卵管癌/原发腹膜癌，腹腔冲洗液或腹水阳性）。
③将淋巴结转移由ⅢC 期更改为ⅢA 1 期，原ⅢA 期（镜下盆腔外腹膜转移）改为ⅢA2 期。
④IV 期进一步分为ⅣA 期（胸水阳性）和ⅣB 期（实质转移、腹腔外脏器包括腹股沟淋巴结、腹腔外淋巴结转移及肿瘤侵犯肠壁全层）。
见下表ⅡⅡA ⅡB ⅢⅢⅢⅢⅢⅢⅢⅢ三、病理类型近年研究表明，上皮性卵巢癌是一组具有显著异质性的疾病，包括多种组织起源及分子遗传学改变各不相同的病理亚型。
总体将卵巢癌分为两型。
I 型：低级别浆液性癌、透明细胞癌、低级别内膜样癌、粘液性癌。
Ⅱ型：高级别浆液性癌、高级别内膜样癌、癌肉瘤、未分化癌。
四、初始治疗(肿瘤内科治疗应当严格掌握临床适应症，并在肿瘤内科医生的指导下施行）卵巢癌初始治疗以分期/减瘤手术及铂类为基础的化疗组成。
减瘤满意度及化疗敏感性是影响其预后的重要因素。
同时，部分早期年轻患者可考虑保留生育功能手术。
（一）、手术治疗：1、早期患者（1）全面分期手术主要包括全子宫+双附件+大网膜+阑尾切除+腹膜后淋巴结清扫术。
- 1、下载文档前请自行甄别文档内容的完整性，平台不提供额外的编辑、内容补充、找答案等附加服务。
- 2、"仅部分预览"的文档,不可在线预览部分如存在完整性等问题,可反馈申请退款(可完整预览的文档不适用该条件!)。
- 3、如文档侵犯您的权益，请联系客服反馈,我们会尽快为您处理(人工客服工作时间：9:00-18:30)。
卵巢癌、卵管癌和腹膜癌的FIGO分期（2014）
1973年FIGO首次发布卵巢癌、卵管癌和腹膜癌的分期，1988年有过一次修订。
本次为第三个版本。
卵巢癌不是一种单纯的疾病，包括数种临床和病理特点迥异的肿瘤。
大约90%为恶性上皮性癌（carcinomas）。
根据组织学、免疫组化和分子遗传学分析，至少有5种主要类型：高级别浆液性癌（70%），内膜样癌（10%），透明细胞癌（10%），粘液性癌（3%）和低级别浆液性癌（不足5%）。
上述类型占据约98%的卵巢癌类型。
恶性生殖细胞肿瘤（无性细胞瘤，卵黄囊瘤，未成熟畸胎瘤）约占3%，恶性潜能的性索间质肿瘤（主要是颗粒细胞瘤）约占1-2%。
原发性卵管癌和原发性腹膜癌比较罕见，和HGSC有很多相似的临床及形态特点，且主要发生在BRCA1/2遗传变异的女性中。
大量证据发现这些肿瘤主要为卵管起源。
而散发的HGSC则有多种来源可能。
既往“苗勒氏管新生化生（mullerian neometaplasia）”的概念得到更多证据支持。
而绝大部分ECs和CCCs则可能来源于内异症。
新的FIGO分期在2012年10月12日提交至FIGO执行委员会，2周后通过。
表1至表3是建议的具体分期系统。
准确的组织病理诊断对于卵巢癌成功分类及治疗至关重要，不同组织学类型对治疗的反应是不同的。
FIGO委员会选择的这种分类系统，将所有肿瘤类型共享的最相关的预后因素考虑在内。
但是，在诊断和分期的时候，仍应清楚说明具体卵巢癌的组织类型。
目前达成一致的组织学类型包括：
1.上皮性癌（按频率顺序排列）：高级别浆液性癌（HGSC），内膜样癌（EC），
透明细胞癌（CCC），粘液性癌（MC），低级别浆液性癌（LGSC）。
注：移行细
胞癌目前认为是HGSC的一种变异形态；恶性Brenner瘤则被认为是极端罕见的
低级别癌。
2.恶性生殖细胞肿瘤（无性细胞瘤，卵黄囊瘤，未成熟畸胎瘤）。
3.恶性潜能的性索间质肿瘤（主要是颗粒细胞瘤，以及含有异源性肉瘤成分的
Sertoli-Leydig细胞瘤）。
作者最后说：分期如水（Staging should be considered fluid），世界越来越小，更多的研究组织应该一起为更加准确的预后系统而努力奋斗。
表1. 2014年FIGO有关卵巢癌、输卵管癌和腹膜癌的分期系统及相应的TNM。
注1：包括肿瘤蔓延至肝脏和脾脏包膜，但不包括脏器实质的受累。
注2：脏器实质转移属于IVB期。
表2. 卵巢癌、输卵管癌和腹膜癌的分组。
注：1.如有可能就应该标注原发部位。
有些情况下可能无法明确说明原发部位，即“未明确部位的（undesignated）”。
2.应该记录组织学类型。
3.分期包括对III期的修订。
分配至IIIA1期的情况基于肿瘤播散至腹膜后淋巴结但没有
腹腔内播散，因为对这些患者的分析发现她们的生存显著优于那些有腹腔内转移的情况。
4.腹膜后淋巴结的受累必须通过组织学或细胞学确诊。
5.从大网膜转移至脾脏或肝脏的情况（IIIC期）应该和那些脾脏或肝脏实质孤立转移的
情况（IVB期）相鉴别。
表3. 对分期改变的解释。