Imatinib is a competitive tyrosine kinase inhibitor used for cancer treatment. Chemotherapy induces c-Abl mediated upregulation of tumor suppressor protein p63 (a homolog of p53) with resultant apoptosis. Rodent studies show that when given prior to cisplatin, imatinib is a potent inhibitor of c-Abl mediated upregulation and blocks apoptosis of cells. Mice treated with imatinib prior to cisplatin show reduced primordial follicular loss and normal progeny [11, 12]. However other studies show no protection with Imatinib in two independent mice strains
. Additionally, the authors show that genetic effects on the oocyte result in early embryonic mortality and marked aneuploidy. There remain concerns regarding whether imatinib and cisplatin treated oocytes that do not undergo apoptosis harbor DNA damage that may result in miscarriage or birth defects [14, 15]. The question also remains whether imatinib reduces the efficacy of cisplatin on the primary tumor target while upregulating the effects of cisplatin in other cell types .