Exploration of molecular targets for endometriosis-associated ovarian cancer with in vitro multistep carcinogenesis model

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To more understand the molecular mechanisms of ovarian carcinogenesis arising from ovarian endometrioma, we first established the immortalized epothelial cells from ovarian endometrioma via overexpressing cyclinD1/cdk4/hTERT cDNA. Based on the genetic analyses of clinical samples, we introduced several genetic factors into these cells to observe the transformed phenotypes. Introduction of dominant negative p53, oncogenic K-ras alleles, together with c-myc overexpression, enabled cells to obtain transformed phenotypes. These 3 steps appeared to be essential for ovarian carcinogenesis associated with endometriosis and thereby will be a promissing molecular target for the novel treatment modality.