Verit Fatma Ferda, Yucel Oguz
Department of Obstetrics and Gynecology, Research and Training Hospital, Infertility Research and Treatment Center, Suleymaniye Maternity, Istanbul, Turkey E-mail :
Asian Pac J Cancer Prev. 2013;14(10):5589-97. doi: 10.7314/apjcp.2013.14.10.5589.
The aim of this review article was to evaluate the relationship and the possible etiological mechanisms between endometriosis, leiomyoma (LM) and adenomyosis and gynecological cancers, such as ovarian and endometrial cancer and leiomyosarcoma (LMS). MEDLINE was searched for all articles written in the English literature from July 1966 to May 2013. Reports were collected systematically and all the references were also reviewed. Malignant transformation of gynecologic benign diseases such as endometriosis, adenomyosis and LM to ovarian and endometrial cancer remains unclear. Hormonal factors, inflammation, familial predisposition, genetic alterations, growth factors, diet, altered immune system, environmental factors and oxidative stress may be causative factors in carcinogenesis. Early menarche, low parity, late menopause and infertility have also been implicated in the pathogenesis of these cancers. Ovarian cancers and endometriosis have been shown to have common genetic alterations such as loss of heterozygosity (LOH), PTEN, p53, ARID1A mutations. MicroRNAs have also been implicated in malignant transformation. Inflammation releases proinflammatory cytokines, and activates tumor associated macrophages (TAMS) and nuclear factor kappa b (NF-KB) signaling pathways that promote genetic mutations and carcinogenesis. MED12 mutations in LM and smooth muscle tumors of undetermined malignant potential (STUMP) may contribute to malignant transformation to LMS. A hyperestrogenic state may be shared in common with pathogenesis of adenomyosis, LM and endometrial cancer. However, the effect of these benign gynecologic diseases on endometrial cancer should be studied in detail. This review study indicates that endometriosis, LM, adenomyosis may be associated with increased risk of gynecological cancers such as endometrial and ovarian cancers. The patients who have these gynecological benign diseases should be counseled about the future risks of developing cancer. Further studies are needed to investigate the relationship between STUMPs, LMS and LM and characteristics and outcome endometrial carcinoma in adenomyotic patients.
这篇综述文章的目的是评估子宫内膜异位症、平滑肌瘤（LM）和子宫腺肌病与妇科癌症（如卵巢癌、子宫内膜癌和平滑肌肉瘤（LMS））之间的关系及可能的病因机制。检索了MEDLINE中1966年7月至2013年5月期间发表的所有英文文献。系统收集报告并查阅所有参考文献。子宫内膜异位症、子宫腺肌病和LM等妇科良性疾病向卵巢癌和子宫内膜癌的恶性转化仍不明确。激素因素、炎症、家族易感性、基因改变、生长因子、饮食、免疫系统改变、环境因素和氧化应激可能是致癌的因素。月经初潮早、低生育力、绝经晚和不孕也与这些癌症的发病机制有关。卵巢癌和子宫内膜异位症已被证明存在共同的基因改变，如杂合性缺失（LOH）、PTEN、p53、ARID1A突变。微小RNA也与恶性转化有关。炎症释放促炎细胞因子，并激活促进基因突变和致癌作用的肿瘤相关巨噬细胞（TAMS）和核因子κB（NF-KB）信号通路。LM和未确定恶性潜能的平滑肌肿瘤（STUMP）中的MED12突变可能导致向LMS的恶性转化。子宫腺肌病、LM和子宫内膜癌的发病机制可能存在共同的高雌激素状态。然而，应详细研究这些妇科良性疾病对子宫内膜癌的影响。这项综述研究表明，子宫内膜异位症、LM、子宫腺肌病可能与子宫内膜癌和卵巢癌等妇科癌症风险增加有关。患有这些妇科良性疾病的患者应被告知未来患癌的风险。需要进一步研究来调查STUMPs、LMS和LM之间的关系以及子宫腺肌病患者子宫内膜癌的特征和预后。
