Chien Jeremy R, Aletti Giovanni, Bell Debra A, Keeney Gary L, Shridhar Viji, Hartmann Lynn C
Department of Experimental Pathology, Mayo Clinic, Rochester, Minnesota, USA.
J Cell Biochem. 2007 Dec 1;102(5):1117-29. doi: 10.1002/jcb.21552.
Ovarian cancer, the most aggressive gynecologic cancer, is the foremost cause of death from gynecologic malignancies in the developed world. Two primary reasons explain its aggressive behavior: most patients present with advanced disease at diagnosis, and die of recurrences from disease that has become resistant to conventional chemotherapies. In this paper on epithelial ovarian cancer (EOC), we will review molecular alterations associated with the few precursor lesions identified to date, followed by the more commonly recognized processes of de novo carcinogenesis, metastasis, and the development of chemoresistance. We will propose a unifying model of ovarian epithelial tumorigenesis that takes into account various hypotheses. We will also review novel approaches to overcome the major problem of chemoresistance in ovarian cancer. Finally, we will discuss advances and new challenges in the development of mouse model systems to investigate EOC precursor lesions, progression, metastasis, and chemoresistance.
卵巢癌是最具侵袭性的妇科癌症，在发达国家是妇科恶性肿瘤致死的首要原因。其侵袭性有两个主要原因：大多数患者在诊断时已处于疾病晚期，且死于对传统化疗产生耐药性的复发性疾病。在这篇关于上皮性卵巢癌（EOC）的论文中，我们将回顾与迄今已确定的少数前驱病变相关的分子改变，随后探讨更常见的新发致癌、转移及化疗耐药发生过程。我们将提出一个综合各种假说的卵巢上皮肿瘤发生统一模型。我们还将回顾克服卵巢癌化疗耐药这一主要问题的新方法。最后，我们将讨论在开发用于研究EOC前驱病变、进展、转移及化疗耐药的小鼠模型系统方面取得的进展和面临的新挑战。
