p53 and Ralbp1 in Carcinogenesis

Dear Colleagues,  

In humans, genetic lesions that cause loss of TP53, a stress-responsive tumor suppressor protein, causes the Li-Fraumeni hereditary cancer syndrome in humans. Spontaneous cancer develop in nearly all TP53-null mice before 6 months of age. In stark contrast, mice lacking the stress-responsive mercapturic acid pathway ATPase enzyme Ralbp1 (which encodes the 76 kDa protein, RLIP76 aka Rlip) are resistant to carcinogenesis even upon exposure to the most potent chemical carcinogens. We discovered that haploinsufficiency of Rlip can switch off spontaneous carcinogenesis in p53 null mice and cause reversion of their gene promoter methylation defects to wild-type. Because of the pleiotropic functions of both p53 and Rlip, the mechanism of this observations remain unclear. Thus, we have invited scientists studying the various functions and cancer signaling pathways linked to Rlip and p53 to contribute to a discussion that may help elucidate the underlying molecular mechanisms.

Prof. Dr. Sanjay Awasthi
Guest Editor

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