We propose that a dysfunctional p53 pathway might be a contributor to occurrence of this state, as the various ovarian cancer cell lines and the SV40 large T-antigen transformed lung epithelial cell line (16HBE) that exhibited the hyperploid response all shared a commonality in p53 alteration as opposed to the non-transformed gingival fibroblast cell line (HGF-1) (Supplementary Figure 7P–7Q). Here, TP53 is linked to ovarian carcinoma.