Figure 2.

Potential therapeutic targets to block PGCC formation during infection with oncoviruses. As a growing body of evidence is pointing toward a crucial role of polypoid giant cancer cells in enhancing tumor evolution and the acquisition of therapy resistance, therapeutically targeting those cells is of utmost importance. Pharmacological modulators of metabolic pathways and AMP kinase activity stimulators appear to be promising candidates that specifically target polyploid tumor cells to counteract tumor repopulation. However, as oncogenic viruses might be mediators and/or inducers of PGCC formation, targeting those pathogens could also constitute a potential therapeutic strategy to block the formation of giant cells, which could disrupt the adaptive capacity of tumors in vivo and establish an effective strategy in the war against cancer. EBV nuclear antigen (EBNA), EMT (epithelial-to-mesenchymal transition) large HBV surface protein (LHBs), latency-associated nuclear antigen (LANA), latent membrane protein 1 (LMP1).