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Activation of NOTCH signaling via DLL1 is mediated by APE1-redox-dependent NF-B activation in oesophageal adenocarcinoma

Liquid biopsy pipeline to inform immuno-oncology trials

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While early literature suggested that p53-dependent tumor suppression involved the induction of cell cycle arrest, senescence or apoptosis, the recent analysis of several transactivation-defective p53 mutants has called this model into question and it now appears that alterations in intracellular metabolism may account for the ability of p53 to suppress tumor formation [6870]