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女性生殖系统恶性中胚叶混合瘤50例临床病理特征

Clinicopathological features of malignant mixed mesodermal tumor: analysis of 50 cases

摘要:

目的:探讨发生在女性生殖系统的恶性中胚叶混合瘤(malignant mixed mesodermal tumor,MMMT)的临床病理学特征、免疫组织化学及分子遗传学特点。方法:收集解放军总医院第一医学中心病理科2005—2019年诊断为恶性中胚叶混合瘤的临床病理资料,分析其组织病理学特点,并通过免疫组织化学法检测雌激素(ER)、孕激素(PR)、p16、p53、错配修复蛋白(MMR)等指标的表达。结果:本组MMMT病例的发生部位包括子宫原发29例、卵巢原发16例、子宫和卵巢双原发4例、宫颈1例。镜下可见肿瘤由癌和肉瘤两种成分构成,分界清楚或相互混合。癌成分在整个肿瘤中占5%~90%不等,其中大部分病例以癌为主,少部分病例癌成分低于50%,其中2例低于10%。癌的类型大多为一种类型,有7例由2种类型的癌混合而成。子宫原发MMMT以子宫内膜样癌居多(55%,16/29),卵巢MMMT以浆液性癌居多(12/16),宫颈MMMT为鳞状细胞癌成分,其他为透明细胞癌、未分化癌。肉瘤的类型,同源性肉瘤包括内膜间质肉瘤、平滑肌肉瘤以及高级别梭形细胞肉瘤,多见于子宫MMMT(72.4%,21/29);异源性肉瘤(包括软骨肉瘤、骨肉瘤及横纹肌肉瘤),多见于卵巢MMMT(12/16);其中10例由2种类型的肉瘤混合而成。子宫卵巢同步发生肿瘤的形态和类型大致相同。直接蔓延或转移性肿瘤(卵巢、子宫、淋巴结、网膜、肠壁、皮肤)均为与主体肿瘤大致相同类型的癌。免疫组织化学ER和PR为双阴性(子宫肿瘤23/25,卵巢肿瘤8/10);p16弥漫强阳性(子宫肿瘤11/11,卵巢肿瘤6/6)。p53多为突变型表达(64%,21/33),在癌和肉瘤成分表达同步;在上皮成分为子宫内膜样癌的病例中,p53突变型表达占35%,在非子宫内膜样癌中占46.7%;在异源性肉瘤的病例中占31.8%,而非异源性肉瘤中占50%。28例(28/33,85%)表现为错配修复蛋白完整,仅5例(5/33,15%)表现为错配修复蛋白缺陷。结论:女性生殖系统MMMT是高级别癌和肉瘤构成的双相性肿瘤,形态复杂多样,免疫组织化学具有ER/PR阴性、p16弥漫强阳性的特点,多为p53突变型和MMR完整。

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abstracts:

Objective:To investigate the clinicpathological, immunohistochemical and molecular genetic features of malignant mixed mesodermal tumor (MMMT) in the female reproductive system.Methods:To analyze its histopathological characteristics, we performed a retrospective review of the MMMT cases diagnosed at PLA General Hospital, Beijing, China during 2005-2019 using its surgical and pathological databases. EnVision immunohistochemical staining was used to detect the expression of ER, PR, p16, p53 and MMR proteins.Results:Fifty cases were conformed to the diagnosis, including 29 cases originated in the uterus, 16 cases in ovary, 4 cases of synchronous occurrence in uterus and ovary, 1 case in cervix. The tumor was histologically composed of two components, namely carcinoma and sarcoma ones, with clear borderline or blend mutually. The proportion of cancer component in the whole tumor ranged from 5%-90%. The proportion of carcinoma was more than 50% in 76% of the cases, and less than 50% in 24% of cases, including 2 cases with<10% of carcinoma. In the cases of primary uterine MMMT, the main carcinoma type was high grade endometrioid carcinoma (55%, 16/29). In ovarian MMMT, the main carcinoma type was serous carcinoma (12/16), while that of cervical MMMT was squamous cell carcinoma. The others were clear cell carcinoma or the undifferentiated carcinoma. There was one carcinoma type in most cases, only 7 cases had two carcinoma types. Homologous sarcomas, including stromal sarcoma, leiomyosarcoma and high-grade spindle cell sarcomas, were more commonly found in uterine MMMT (72.4%, 21/29). While heterogenic sarcomas, including chondrosarcoma, osteosarcoma and rhabdomyosarcoma, were more commonly noted in ovarian MMMT (12/16) than MMMT of other sites. There were 10 cases that consisted of two types of sarcomas. The synchronous MMMT of uterus and ovary had similar morphology and the types of carcinoma and sarcoma. The tumor cells that spread or metastasized to lymph node, omentum, intestinal wall or skin were all carcinoma cells, and were morphologically consistent with the original tumors. Immunohistochemically, ER and PR were both negative (23/25 in uterine, 8/10 in ovarian tumors). p16 was strongly positive (11/11 in uterine tumors, and 6/6 in ovarian tumors), with similar expression patterns in the carcinoma and sarcoma components. p53 showed mutant-type staining (64%, 21/33) and expressed synchronously in carcinoma and sarcoma components. p53 mutation was found in 35% cases of endometrial carcinoma and 46.7% cases of non-endometrial carcinoma. p53 mutation was also found in only 31.8% cases of heterogenic sarcomas, but in 50% of non-heterogenic sarcomas. Twenty-eight cases (28/33, 85%) presented intact mismatch repair proteins, while 5 cases (5/33, 15%) presented deficient mismatch repair proteins.Conclusions:MMMT in female reproductive system is a rare high-grade biphasic tumor with complex and diverse morphology. The immunohistochemical features are characterized by negative ER/PR and strongly positive p16, mostly mutant p53 and proficient mismatch repair proteins. The patients with a high FIGO stage have worse prognosis.

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