Department of Obstetrics and Gynecology, U.T.M.B. Galveston Branch, 301 University Blvd, Galveston, TX 77555, USA.
Horm Cancer. 2010 Dec;1(6):277-90. doi: 10.1007/s12672-010-0054-2.
Multiple genetic alterations play a role in the pathogenesis of ovarian cancer. Although many key proteins and pathways involved in ovarian carcinogenesis and metastasis have been discovered, knowledge of the early steps leading to malignancy remains poorly understood. This poor understanding stems from lack of data from early-stage cancers and absence of a well-established premalignant state universal to all ovarian cancer subtypes. Existing evidence suggests that ovarian cancers develop either through a stepwise mutation process (low-grade pathway), through genetic instability resulting in hastened metastasis (high-grade pathway), or more recently through what has been described as the "'fimbrial-ovarian' serous neoplasia theory." In this latter model, ovarian serous cancers evolve from premalignant lesions in the distal fallopian tube called tubal intraepithelial carcinoma. In this manuscript, we review key genetic and molecular changes that occur in cancer cell progression and suggest a model of ovarian cancer pathogenesis involving both tumor cell mutations and microenvironmental factors.
多种基因改变在卵巢癌的发病机制中起作用。尽管已经发现了许多涉及卵巢癌发生和转移的关键蛋白质和途径,但导致恶性肿瘤的早期步骤的知识仍知之甚少。这种理解上的欠缺源于缺乏早期癌症的数据以及缺乏适用于所有卵巢癌亚型的公认的癌前状态。现有证据表明,卵巢癌的发生要么是通过逐步突变过程(低级别途径),要么是由于遗传不稳定性导致转移加速(高级别途径),或者最近是通过所谓的““‘纤毛-卵巢’浆液性肿瘤理论”。在后一种模型中,卵巢浆液性癌起源于称为输卵管上皮内癌的输卵管远端的癌前病变。在本文中,我们回顾了癌症细胞进展中发生的关键遗传和分子变化,并提出了一个涉及肿瘤细胞突变和微环境因素的卵巢癌发病机制模型。