Doxorubicin, through its planar anthracycline core and an amino sugar moiety exerts its antitumor effects through DNA intercalation, free radical generation and stabilization of topoisomerase II–DNA complexes, compromising genomic integrity and promoting apoptosis. These mechanisms sensitize tumor cells to OV infection. In doxorubicin-resistant ovarian cancer, suppression of the MEK-ERK pathway enhances viral replication and cytotoxicity, supporting the therapeutic potential of combining doxorubicin with OVT. Here, MAP2K7 is linked to neoplasm.