卵巢子宫内膜异位症恶变的临床病理特征分析

目的:分析卵巢子宫内膜异位症(EMs)恶变的临床病理特征。方法:回顾分析2011年12月至2015年12月于郑州大学人民医院妇科行手术治疗且术后病理确诊的卵巢癌患者281例,其中符合内异症恶变诊断标准者24例(内异症恶变组),非内异症恶变者257例(非内异症恶变组)。分析两组患者的临床组织病理学类型及FIGO分期。结果:与非内异症恶变组相比,内异症恶变组患者的平均年龄早、绝经前诊断比例较大,差异均有统计学意义(P0.05)。内异症恶变组术前CA125值(110.27±112.62)U/ml,腹水量较少、病理类型多为透明细胞癌(45.83%)、FIGO分期早期(87.50%);非内异症恶变组术前CA125值(1242.75±2104.28)U/ml、腹水量较多,病理类型多为浆液性腺癌(72.37%),FIGO分期晚期(74.71%);两组比较,差异均有统计学意义(P均0.05)。两组患者在癌灶单双侧及淋巴结转移情况比较,差异均无统计学意义(P均0.05)。结论:卵巢内异症恶变患者发病年龄小、腹水量少、术前CA125较低、FIGO期别早,组织病理以透明细胞癌及子宫内膜样腺癌为主。     

子宫内膜异位症相关性卵巢癌的研究现状及展望

子宫内膜异位症(内异症)是最常见的妇科疾病之一。内异症恶变与卵巢透明细胞癌和卵巢子宫内膜样癌存在密切联系,甚至被认为是后者的癌前病变。既往临床研究显示内异症相关性卵巢癌(endometriosis associated ovarian carcinoma,EAOC)患者有某些特殊的临床病理特点,预后相对较好;基础研究发现某些特殊的基因异常表达与其相关。后续研究应着重于从EAOC发现新的分子分型靶点,以便指导临床筛选内异症恶变高危人群、预测疾病进展、实现此类卵巢癌的精准分型和分层管理。     

卵巢上皮性癌合并卵巢子宫内膜异位症67例临床病理分析

目的 探讨合并卵巢子宫内膜异位症(内异症)的卵巢上皮性癌(卵巢癌)的临床病理特点.方法 选取1996年1月至2006年12月在复旦大学附属妇产科医院就诊并经手术确诊的卵巢癌共727例,对其中合并卵巢内异症的67例患者(其中由卵巢内异症恶变的卵巢癌患者34例,为A组;其他仅合并卵巢内异症的卵巢癌患者33例,为B组)的临床病理资料进行回顾性分析,并与660例未合并卵巢内异症的卵巢癌患者(C组)进行对照分析.同期本院经手术病理确诊的卵巢内异症患者共3890例.结果 卵巢内异症恶变为卵巢癌的发生率为0.87%(34/3890).卵巢癌合并卵巢内异症的发生率为9.2%(67/727).A、B、C组患者的平均年龄分别为(47.2±1.3)、(47.8±1.2)、(51.2±0.4)岁,3组问比较,差异有统计学意义(P=0.013).A、B组病理类型多为透明细胞癌(分别为67.6%、69.7%),其所占比例均明显高于C组的18.8%(P=0.000);而C组以浆液性腺癌(50.3%)为主,其所占比例明显高于A组的8.8%和B组的12.1%(P=0.000).A、B组手术病理分期多为Ⅰ期(分别为73.5%、63.6%),其所占比例均明显高于C组的31.4%(P=0.000);而C组多为Ⅲ期(47.7%),其所占比例明显高于A组的23.5%和B组的15.2%(P=0.001).A、B、C组高分化(分别为11.8%、6.1%、10.5%)、中～低分化(分别为88.2%、93.9%、89.5%)所占比例分别比较,差异均无统计学意义(P=0.602).A、B、C组雌激素受体(ER)阳性率分别为22.2%(6/27)、31.6%(6/19)、43.9%(136/310),3组间比较,差异有统计学意义(P=0.018);A、B、C组孕激素受体(PR)阳性率分别为22.2%(6/27)、15.8%(3/19)、35.5%(110/310),3组间比较,差异无统计学意义(P=0.082).患者总的5年累积生存率为55.6%,A、B、C组患者的5年累积生存率分别为78.9%、92.8%、51.9%,3组间比较,差异有统计学意义(P=0.000).结论 合并卵巢内异症的卵巢癌患者,具有年轻(尤其是内异症恶变患者)、多为卵巢透明细胞癌、期别早、ER表达水平低、预后好的特点.     

卵巢子宫内膜异位症恶变研究的新进展

本文主要从流行病学和发病机制两方面综述了近年卵巢子宫内膜异位症恶变研究的新进展。流行病学方面,通过内异症相关卵巢癌发病率和卵巢癌中内异症的发病率介绍了两者间的联系。发病机制方面,主要介绍了有关杂合性丢失、表观遗传异常、信号传导通路、生长因子/炎症因子异常等的内容。     

卵巢子宫内膜异位症恶变26例临床病理分析

目的 探讨探讨卵巢子宫内膜异位症（内异症）恶变的临床病理特征。方法 回顾分析26例卵巢内异症恶变患者的临床和病理资料。结果 患者以痛经和检查发现盆腔肿块为主要临床表现。行B超或彩色多普勒超声检查者18例,其中10例发现盆腔肿块中含实质性结构。肿瘤组织类型以内膜样腺癌和透明细胞癌常见。58％（15／26）患者的肿瘤显微镜下可见不典型内异症。协际妇产科联盟分期：Ⅰ期21例（81％）,Ⅱ期3例（12％）,Ⅲ期2例（8％）。结论 卵巢内异症恶变早期临床诊断存在困难,B超或彩色多普勒超声检查有重要参考价值。重视观察异位内膜组织形态变化,有利于认识卵巢内异症恶变的发生和发展过程,提高诊断和治疗水平。     

子宫内膜异位症长期管理的思索——绝经后内异症

子宫内膜异位症简称内异症，是一种雌激素依赖性疾病，传统上被认为发生于绝经前女性，疾病随着卵巢功能的衰竭而“治愈”。内异症应长期管理，目前国内外指南均按青春期、育龄期、围绝经期对该病分年龄阶段综合治疗给予详细论述。近年来不断有文献报道绝经后内异症，包括绝经前内异症病灶经长期管理至绝经后依旧持续存在甚至进展，以及绝经后新发现的内异症病灶。绝经后内异症的发病机制仍待探索，而疾病在此年龄段的特殊性及恶变风险更需接受规范化管理及治疗。目前针对绝经后内异症尚无明确的管理细则。本综述旨在回顾分析国内外研究，对绝经后内异症的临床特点、治疗及管理策略进行探索和讨论。     

子宫内膜异位症

主要讨论内容1.在位内膜在子宫内膜异位症(内异症)发病机制中的地位2.内异症的临床病理类型、病变特点与临床症状的关系3.内异症手术治疗的进展和争议4.内异症药物治疗的现状及前景5.内异症不育的相关因素和治疗策略6.内异症恶变问题7.内异症患者绝经后激素替代的现代观8.内异症复发的诊断及治疗在位内膜在内异症发病机制中的地位郎景和教授内异症的发病机制不清。近百年来以Sampson的经血逆流种植学说为主导理论,但经血逆流是妇女月经期常见的现象,可发生于80%~90%的月经周期,但临床上仅10%~15%育龄妇女罹患内异症,这是Sampson学说无法解…     

SPOCK2基因表观失活在卵巢子宫内膜异位症恶变中的作用

目的 通过比较卵巢子宫内膜异位症(内异症)恶变患者的恶变组织、异位内膜组织和在位内膜组织中SPOCK2基因的甲基化及蛋白表达情况,探讨该基因的表观失活在卵巢内异症恶变中的作用.方法 选择2005年1月至2011年1月在中国医科大学附属盛京医院妇产科住院手术、并经术后病理确诊为卵巢内异症恶变患者22例的病理石蜡标本为恶变组(包括11例卵巢内膜样癌、8例透明细胞癌、2例浆液性囊腺癌及1例黏液性囊腺癌),以同期22例单纯卵巢内异症患者的异位内膜及在位内膜的病理石蜡标本(内异症组)及16例宫颈上皮内瘤变(CIN)Ⅲ患者的正常子宫内膜的病理石蜡标本(对照组)为对照.通过显微切割技术分别获取恶变组患者的恶变组织22份,癌旁异位内膜组织15份及在位内膜组织10份;内异症组患者的异位内膜组织22份及在位内膜组织17份;对照组患者的正常子宫内膜组织16份.通过亚硫酸盐修饰后酶切技术检测各组织中SPOCK2基因甲基化情况,免疫组化SP法检测SPOCK2基因的蛋白表达情况.探讨SPOCK2基因异常甲基化与其蛋白表达的关系.结果 (1)SPOCK2基因甲基化情况:恶变组患者的恶变组织中,SPOCK2基因甲基化发生率为45％(10/22),显著高于癌旁异位内膜组织(1/15),两者比较,差异有统计学意义(P＜0.05);恶变组患者的癌旁内异症组织中SPOCK2基因甲基化发生率(1/15)与内异症组患者的异位内膜(5％,1/22)比较,差异无统计学意义(P＞0.05).(2)SPOCK2基因蛋白表达情况:恶变组患者的恶变组织中SPOCK2基因蛋白表达缺失率为44％(11/22),显著高于恶变组患者癌旁异位内膜组织的2/15,两者比较,差异有统计学意义(P＜0.05);但恶变组患者癌旁异位内膜组织中SPOCK2基因蛋白表达缺失率(2/15)与内异症组异位内膜(5％,1/22)比较,差异无统计学意义(P＞0.05).3组在位内膜组织中SOPCK2基因的蛋白表达缺失率比较,差异无统计学意义(P＞0.05).(3)SPOCK2基因甲基化与其蛋白表达缺失的关系:SPOCK2基因异常甲基化能够导致其蛋白表达缺失( 20/22,P＜0.05).结论 SPOCK2基因的表观失活与卵巢内异症恶变相关.     

子宫内膜异位症恶变的研究进展

子宫内膜异位症 (内异症 )具有临床病变的广泛性和病理表现的多形性的特点 ,虽属良性疾病 ,但其表现与恶性肿瘤的生物学行为类似 ,并且有一定比例的内异症发生组织学改变 ,成为癌瘤[1 ] 。因此 ,内异症的恶变及其与癌瘤的关系日趋受到关注 ,并对研究内异症有重要意义。一、内异症的恶性行为和恶变1.内异症的生物学行为 :内异症具有与恶性疾病相似的表现 ,如局部浸润或远处转移 ,与周围组织严重粘连 ,对其他组织或器官侵袭和破坏。但内异症病灶中没有癌细胞 ,即内异症恶性表现只限于生物学行为上。2 .内异症恶变组织学上的连续性 :目前内异症…     

绝经后子宫内膜异位症22例临床分析

目的 :探讨绝经后子宫内膜异位症 (内异症 )的临床特点。方法 :回顾性分析我院自1993年 6月至 2 0 0 2年 6月手术证实的 2 2例绝经后内异症患者的临床资料。结果 :患者年龄 4 7～ 6 5岁 ,平均 5 5 .6± 4 .8岁。主要症状有盆腔包块 15例 ,绝经后阴道流血 9例 ,阴道分泌物增多2例 ,慢性盆腔疼痛 1例。 19例 (86 .4 % )术前误诊。 2 2例均行全子宫加双附件切除术。I、II期 3例 ,III、IV期 19例。术后病理证实合并子宫肌瘤 13例 ,子宫腺肌病 7例 ,子宫内膜癌 2例 ,卵巢癌 1例。随诊时间超过 6个月的有 12例 ,其中HRT者 7例均无复发。结论 :绝经后内异症很可能是绝经前就存在的。临床表现不典型 ,常常与其他激素依赖性疾病同时存在 ,易于漏诊。全子宫加双附件切除术是诊断及治疗的主要方法。     

子宫内膜异位症与卵巢癌关系的研究进展

子宫内膜异位症(endometriosis,EMs)是一种良性妇科疾病,但具有恶性行为。流行病学及病理学等研究证实EMs可增加卵巢癌,尤其是透明细胞癌和子宫内膜样癌的风险。近年国内外关于EMs相关卵巢癌(endometriosis associated ovarian cancer,EAOC)的报道不断增加,已证实这是一类特定类型的卵巢癌,EAOC的病因、发病机制和临床特点的研究已成为热点。通过阅读大量文献,分析目前报道的EAOC的危险因素、发病机制、临床特点及诊断方法,以提高对该病的认识。     

表观遗传学与子宫内膜异位症相关性卵巢癌发生机制的研究进展

子宫内膜异位症（endometriosis,EMs）指子宫内膜组织在子宫腔外的存在,是一种慢性的、激素依赖性的妇科疾病,影响着全球数百万女性。虽然EMs在形态学上表现为良性,但其在临床行为学上却表现为增生、浸润、复发等恶性肿瘤的特点。已有充分证据表明EMs可通过多种机制增加恶性转化的风险,但目前关于EMs发生恶性转化的具体机制尚不明确。越来越多证据表明,表观遗传修饰不仅参与EMs的发生,而且在EMs恶性转化的发病机制中发挥重要作用,包括DNA甲基化和去甲基化、组蛋白修饰、微小RNA（microRNAs,miRNAs）异常表达等。综述表观遗传学与子宫内膜异位症相关性卵巢癌（endometriosis associated ovarian cancer,EAOC）发生机制的研究进展,以期寻找可能与EMs恶性转化相关的一些危险因素。     

Von der Endometriose zum Ovarialkarzinom

Endometriosis is a common benign disease with a prevalence of about 10% in the female population during the reproductive phase. The risk of developing endometriosis-associated ovarian cancer (EAOC) is doubled for women with endometriosis in comparison to the risk of women without endometriosis developing ovarian cancer. If patients with endometriosis suffer additionally from long lasting infertility, the risk for EAOC is even increased four times. Retrospective studies have shown a histopathological correlation between endometriosis and EAOC. Recent investigations focus on the molecular biological methods used to describe new aspects of the pathophysiology of this disease. The formation of EAOC seems to be influenced by inflammation within the peritoneal cavity, angiogenesis, hyperestrogenism, the aromatase pathway, cyclooxygenae-2 and loss of genetic material such as the inactivation of tumor suppressor genes. Such molecular biological investigations may reduce the incidence of EAOC.     

子宫内膜异位症相关卵巢癌病因研究进展

子宫内膜异位症(endometriosis,EMs)在病理学表现上虽为良性病变,但具有与恶性肿瘤相似的浸润、种植生长、破坏周围组织、远处转移和极易复发的特点,并有一定比例的EMs会发生组织形态学改变,从非典型内膜异位组织进一步转变成癌。目前EMs恶变已受到世界各地学者的广泛关注。EMs和卵巢癌的组织联系虽早已被学者提出,并有公认的诊断标准,但是随着近年来EMs和卵巢癌发病率的增加,子宫内膜异位症相关卵巢癌(endometriosisassociated ovarian cancer,EAOC)愈发引起学者的重视,其病因、发病机制、流行病学特征等已成为近年的研究热点。就近年的研究成果主要从基因突变、细胞凋亡、炎症免疫、氧化应激、雌激素5个方面对EAOC的病因和发病机制进行阐述。     

Endometriosis and malignoma

Malignant tumors arising from endometriosis are rare. A frequency of about 1% has been reported with in 80% the ovary, and in 20% extragonadal sites being affected. The most common extragonadal manifestations are the rectosigmoid and the rectovaginal septum. For extragonadal malignant tumors arising from endometriosis, complete resection followed by post-operative radiotherapy, possibly plus adjuvant progestin therapy, is the treatment of choice. Endometriosis-associated ovarian carcinomas are likely to present with lower stage disease and predominantly lower grade tumors. While their treatment follows that of common ovarian cancer, a poorer response to chemotherapy must be considered. As unopposed estrogen replacement therapy has been identified as a risk factor for the development of endometriosis-associated cancer, it is not recommended for hormone replacement therapy in women with a history of endometriosis. Loss of heterozygosity and mutations of the PTEN tumor suppressor gene may be early events of tumorigenesis. Endometriosis and its malignant transformation, perhaps, may serve as a suitable model in this regard. According to recent studies, endometriosis is associated with an increased relative risk of non-Hodgkin lymphoma.     

Hormonal suppressive therapy for endometriosis may not improve patient health

OBJECTIVE: To critically examine the possible association between hormonal treatment of endometriosis and ovarian cancer. RESULT(S): The malignant potential of endometriosis has been suggested by several clinical studies. Although controversial, ovarian carcinoma of the endometrioid and clear cell subtypes has been associated with endometriosis, particularly among subjects with a longstanding disease. Furthermore, a significantly higher frequency of endometriosis has been found in patients undergoing surgery for endometrioid, clear cell, and mixed subtypes of ovarian carcinoma, as compared with the other subtypes. Changes in the genomic material in endometriotic implants were observed by many investigators in chromosomes 1, 5, 6, 7, 16, and 22 by several methods (fluorescent in situ hybridization, comparative genomic hybridization, and others). Because hormonal ablative treatments may suppress the normal, eukaryotic cells more than the aneuploid cells bearing chromosomal aberrations, it may increase the rate of dyskaryotic cells in the endometriotic implants, possibly augmenting the risk of malignant transformation. A recent published association between Danazol and ovarian cancer suggests that such a theoretical risk may occur. CONCLUSION(S): The hormonal ablative treatment of endometriosis may increase the risk of malignant transformation in the endometriotic implants by causing a negative selection and increasing the rate of dyskaryosis and loss of heterozygosity.     

Endometriosis and the development of malignant tumours of the pelvis. A review of literature

For several decades, endometriosis has been suspected of playing a role in the aetiology of ovarian cancer. The literature concerning a possible histogenesis of ovarian cancer from benign endometriosis is reviewed in this chapter. Epidemiological evidence from large-cohort studies confirms endometriosis as an independent risk factor for ovarian cancer. Further circumstantial evidence for this link was found in the common risk factors for ovarian cancer and endometriosis. These risk factors influence retrograde menstruation and endometriosis in the same positive or negative way. Based on data in the literature, the prevalence of endometriosis in epithelial ovarian cancer has been calculated to be 4.5, 1.4, 35.9, and 19.0% for serous, mucinous, clear-cell and endometrioid ovarian carcinoma, respectively. The risk of malignant transformation in ovarian endometriosis was calculated at 2.5% but this might be an underestimate. In addition, some authors described atypical endometriosis in a spatial and chronological association with ovarian cancer. Finally, molecular studies have detected common alterations in endometriosis and ovarian cancer. These data suggest that some tumours, especially endometrioid and clear-cell carcinomas, can arise from endometriosis. Moreover, endometriosis-associated ovarian cancer represents a distinct clinical entity, with a more favourable biological behaviour, given a lower stage distribution and better survival than non-endometriosis-associated ovarian cancer.     

Endometrioid carcinoma arising in endometriosis. Case report.

Malignant transformation arising in endometriosis has been reported in some cases. Following Sampson's criteria, about 0.7%-1% of all cases of endometriosis undergo malignant transformation and the ovary is the most frequent site. A case is reported of a patient with endometriosis which, after 10 years, grew into ovarian endometrioid carcinoma. The relationship between endometriosis and cancer suggests a radical treatment of endometriosis and a careful assessment of postmenopausal woman presenting reactivation signs.