Verma et al. 2010 observed that treatment with 20μm N3a (four times more than our treatment) can cause the formation of double strand DNA strand breaks and initiate a p53-independent DDR in colon cancer cell model characterized by the phosphorylation of H2AX (Ser-139) and p53 (Ser-15), but the DDR was higher in cells exhibiting p53 stabilization. This evidence concerns the gene H2AX and colonic neoplasm.