H2AX and neoplasm: DNA damage induced by chemotherapeutic agents results in rapid phosphorylation of histone H2AX at Ser139, which promotes cellular apoptosis.43, 44 The data demonstrated that HCT116 cells expressing IGPR-1 had significantly less γH2AX in response to doxorubicin treatment compared to control cells (Figure 6b), indicating that expression of IGPR-1 in tumor cells acts to delay or suppress the damage caused by doxorubicin.