Neda Slade

TL;DR: The experiments test the hypothesis that chronic dietary poisoning by aristolochic acid is responsible for EN and its associated urothelial cancer and conclude that dietary exposure to AA is a significant risk factor for ENand its attendant transitional cell cancer.

TL;DR: The tumor suppressor p53 is critically important in the cellular damage response and is the founding member of a family of proteins as discussed by the authors, which regulate cell cycle and apoptosis after DNA damage, and despite a remarkable structural and partly functional similarity among p53, mouse knockout studies revealed an unexpected functional diversity among them.

TL;DR: Deregulated expression of ΔNp73 can bestow oncogenic activity upon the TP73 gene by functionally inactivating the suppressor action of p53 and TAp73 via a dominant-negative family network.

TL;DR: Dietary exposure to aristolochic acid is causally related to endemic nephropathy and carcinomas of the upper urinary tract and TP53 mutations in tumor tissues are identified by chip sequencing.

TL;DR: It is found that the set of NH2-terminal p73 isoforms distinguishes ovarian cancer patients from healthy controls and thus is a molecular marker for this diagnosis, and strongly supports the hypothesis that overexpression of transdominant p 73 isoforms can function as epigenetic inhibitors of p53 in vivo, thereby alleviating selection pressure for p53 mutations in tumors.