MOAP-1, UBR5 and cisplatin resistance in ovarian cancer

Scott T. Eblen, Amber Bradley


Over 22,000 American women are diagnosed with ovarian cancer each year and 14,000 die of this disease, making it the fifth leading cause of cancer deaths among women and the number one gynecological cancer. Ovarian cancer is primarily treated with surgical debulking and chemotherapy that includes a taxane, such as paclitaxel or docetaxel, which interferes with the breakdown of the mitotic spindle during mitosis, and a platinum-based DNA-damaging agent, such as cisplatin or carboplatin. Due to relatively facile peritoneal dissemination of ovarian cancer cells, chemotherapy is of major importance in eliminating peritoneal micrometastases. Most patients with serous ovarian cancer initially respond to treatment, causing the disease to enter remission, but tumors often develop resistance to chemotherapy upon subsequent recurrences. Determining the mechanisms of platinum and taxol resistance is important to understanding disease progression and identifying novel therapeutic targets and strategies. Platinum resistance occurs through many mechanisms, including upregulation of DNA repair mechanisms, enhanced drug efflux from cells and downregulation of the cellular response to apoptosis, among others (1).