H2AX and neoplasm: Immunoblotting of tissue samples from tumor-bearing organotypic slice cultures post treatment revealed that AZ-1 single treatment efficiently reduced FANCD2 protein abundance, and upon co-treatment with CPPD, SCC tumors lost FANCD2 and significantly upregulated ɣ-H2AX along with pro-apoptotic signaling, as seen by Caspase 9 cleavage, when compared to CPPD single treatment (Fig. 7I).