Berek J S, Martínez-Maza O
Department of Obstetrics and Gynecology, University of California, Los Angeles Medical Center 90024.
J Reprod Med. 1994 Apr;39(4):241-8.
The development and progression of epithelial ovarian cancer can be correlated with various biologic and molecular factors. Tumor growth has been associated with aberrant and dysfunctional expression and mutation of various genes. These genetic defects include oncogene overexpression, amplification or mutation, aberrant tumor suppressor gene expression or mutation, and the inappropriate expression of cytokines and growth factors and/or the cellular receptors for these molecules. Dysregulation of host immune responses may also play a permissive role in the pathogenesis of the disease. Since ovarian cancer has been associated with the frequency of ovulation, the repeated proliferation of epithelial cells may increase the chance of a genetic accident that could contribute to the activation of an oncogene or inactivation of a suppressor gene. These events, combined with the inherent ability of ovarian epithelial cells to respond to and produce various cytokines and growth factors, could promote oncogenesis.
上皮性卵巢癌的发生和发展与多种生物学和分子因素相关。肿瘤生长与各种基因的异常和功能失调表达及突变有关。这些基因缺陷包括癌基因的过度表达、扩增或突变,肿瘤抑制基因的异常表达或突变,以及细胞因子、生长因子和/或这些分子的细胞受体的不适当表达。宿主免疫反应的失调在该疾病的发病机制中也可能起促进作用。由于卵巢癌与排卵频率有关,上皮细胞的反复增殖可能增加基因意外事件的发生几率,这可能导致癌基因激活或抑癌基因失活。这些事件,再加上卵巢上皮细胞对各种细胞因子和生长因子作出反应并产生这些因子的内在能力,可能会促进肿瘤发生。