Risk of carcinoma in women with ovarian endometrioma.

Risk of carcinoma in women with ovarian endometrioma.
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DOI:
10.2741/e267
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发表时间:
2011
期刊:
Frontiers in bioscience
影响因子:
--
通讯作者:
Hiroshi Kobayashi;Hirotaka Kajihara;Yoshihiko Yamada;Y. Tanase;S. Kanayama;N. Furukawa;T. Noguchi;S. Haruta;S. Yoshida;K. Naruse;T. Sado;H. Oi
Hiroshi Kobayashi;Hirotaka Kajihara;Yoshihiko Yamada;Y. Tanase;S. Kanayama;N. Furukawa;T. Noguchi;S. Haruta;S. Yoshida;K. Naruse;T. Sado;H. Oi
中科院分区:
其他
文献类型:
--
作者:
Hiroshi Kobayashi;Hirotaka Kajihara;Yoshihiko Yamada;Y. Tanase;S. Kanayama;N. Furukawa;T. Noguchi;S. Haruta;S. Yoshida;K. Naruse;T. Sado;H. Oi

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据估计,子宫内膜异位症影响着 10% 的育龄妇女。在这里,我们回顾了子宫内膜异位症相关上皮性卵巢癌(EOC)分子起源的最新知识。本文综述了子宫内膜异位症相关 EOC 的生物学、发病机制和病理生理学研究的英文文献。尽管子宫内膜异位症通常仍然是良性病症,但它表现出体细胞获得性遗传改变。透明细胞癌 (CCC) 和子宫内膜样腺癌 (EAC) 是与子宫内膜异位症相关的最常见的 EOC 类型。月经逆行或卵巢出血将铁等高促氧化因子带入腹膜腔或卵巢子宫内膜异位症。在子宫内膜异位症相关 EOC 的研究中应分别考虑 CCC 和 EAC。子宫内膜异位症中反复发生的出血可通过三个主要过程促进癌变和进展:1)氧化应激增加促进DNA甲基化; 2)激活抗凋亡途径支持肿瘤生长; 3)应激信号通路的异常表达有助于肿瘤进展。这篇综述总结了对子宫内膜异位症相关 EOC 的流行病学、致癌作用、发病机制和病理生理学的最新进展;并提出了一种可能的新颖模型。
Endometriosis affects an estimated 10% of women in the reproductive-age group. Here, we review current knowledge on molecular genesis of endometriosis-associated epithelial ovarian carcinoma (EOC). This article reviews the English language literature for biology, pathogenesis, and pathophysiological studies on endometriosis-associated EOC. Although endometriosis generally remains a benign condition, it demonstrates somatically acquired genetic alterations. Clear cell carcinoma (CCC) and endometrioid adenocarcinoma (EAC) are the most frequent types of EOC associated with endometriosis. Retrograde menstruation or ovarian hemorrhage carries highly pro-oxidant factors, such as iron, into the peritoneal cavity or ovarian endometrioma. CCC and EAC should be considered separately in studies of endometriosis-associated EOC. The repeated events of hemorrhage in endometriosis can contribute to carcinogenesis and progression via 3 major processes: 1) increasing oxidative stress promotes DNA methylation; 2) activating anti-apoptotic pathways supports tumor promotion; and 3) aberrant expression of stress signaling pathways contributes to tumor progression. This review summarizes recent advances in the understanding of epidemiology, carcinogenesis, pathogenesis, and pathophysiology of endometriosis-associated EOC; and a possible novel model is proposed.