Therapeutic implications for ovarian cancer emerging from the Tumor Cancer Genome Atlas

Today, all epithelial ovarian cancers (EOC) are treated with the same approach which involves a debulking surgery and chemotherapy with a carboplatin doublet, usually paclitaxel, for six cycles. These cycles of chemotherapy can be administered in a neoadjuvant, sandwiched, or adjuvant fashion. The outcome is the same and depends on the quality of the debulking and the responsiveness to platinum. Despite an 80% response rate, less than 20% of women will be cured, and most will eventually recur. Patients with recurrent disease are usually incurable. Five year survival for stage III ovarian cancer, the stage at which EOC is commonly diagnosed, is between 35% and 45%. The current combined surgical-chemotherapy approach has reached a plateau of efficacy. Cells protect themselves from environmental and physiological pressures through complex adaptation strategies including cell cycle checkpoints, DNA damage response pathways, programmed cell death (1) and other mechanisms. When imbalance between DNA damage/repair and activation/inactivation occur in these processes, through carcinogenesis or other intrinsic or extrinsic anomalies, cells might become cancerous. These complex adaptation pathways are being discovered through constant molecular biology discoveries, although our understanding remains limited. The TCGA data helps make further inroads in our understanding of the biology of high grade papillary serous ovarian cancer (HGSOC)