Boltz E M, Kefford R F, Leary J A, Houghton C R, Friedlander M L
Department of Medicine, University of Sydney, Westmead Centre, NSW, Australia.
Int J Cancer. 1989 Mar 15;43(3):428-30. doi: 10.1002/ijc.2910430314.
Amplification of the c-ras-Ki oncogene has been the most consistent finding reported in studies on oncogene activation in ovarian cancer, but for the most part the studies have been small and the results conflicting. In order to determine whether amplification occurred de novo in primary tumours or was associated with tumour progression and metastasis, 81 tumour samples from different sites in 26 patients with ovarian tumours and 7 xenografted ovarian tumour cell lines were assayed. Amplification of c-ras-Ki occurred infrequently and was apparent in a single metastatic site in a patient with poorly differentiated serous cystadenocarcinoma of the ovary. Ten-fold amplification of the c-ras-Ki oncogene was also evident in a benign ovarian fibroma. Amplification of the c-ras-Ki oncogene is rare in ovarian tumours and does not appear to play a fundamental role in tumor development or progression.
c-ras-Ki癌基因的扩增是卵巢癌致癌基因激活研究中报道最为一致的发现,但大部分研究规模较小且结果相互矛盾。为了确定扩增是在原发性肿瘤中新生出现的,还是与肿瘤进展和转移相关,对26例卵巢肿瘤患者不同部位的81个肿瘤样本以及7个异种移植的卵巢肿瘤细胞系进行了检测。c-ras-Ki的扩增很少发生,仅在1例低分化卵巢浆液性囊腺癌患者的单个转移部位明显可见。在1例良性卵巢纤维瘤中也明显存在c-ras-Ki癌基因10倍的扩增。c-ras-Ki癌基因在卵巢肿瘤中很少见,似乎在肿瘤发生或进展中不发挥重要作用。