Since polyamines are essential for efficient HR repair [26], a polyamine targeted therapy (such as DFMO with or without a polyamine transport inhibitor) would be predicted to enhance ovarian tumor sensitivity to a PARP inhibitor by impairing critical HR-mediated DNA repair function (upregulated with oncogenic c-MYC, RAS activation, and wild-type BRCA1/2). Here, MYC is linked to ovarian neoplasm.