title: p53 biological network: at the crossroads of the cellular-stress response pathway and molecular carcinogenesis.
abstract: p53 as a key molecular node in the stress response pathway, including inflammation. p53 is involved in several critical pathways including cell cycle arrest, apoptosis, DNA repair, and cellular senescence, which are essential for normal cellular homeostasis and maintaining genome integrity. The alteration of the TP53 gene or posttranslational modification in the p53 protein can alter its response to cellular stress. The molecular archaeology of the TP53 mutation spectrum generates hypotheses concerning the etiology and molecular pathogenesis of human cancer. The spectrum of somatic mutations in the TP53 gene implicates environmental carcinogens, and both endogenous agents and processes in the etiology of human cancer.
authors.affiliation: Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892-4255, USA.
authors.forename: S Perwez
authors.initials: SP
authors.lastname: Hussain
authors.forename: Cutis C
authors.initials: CC
authors.lastname: Harris
mesh_terms: D017209:Apoptosis / Q000502:physiology; D002453:Cell Cycle / Q000502:physiology; D004260:DNA Repair / Q000502:physiology; D016158:Genes, p53 / Q000235:genetics; D006801:Humans; D009369:Neoplasms / Q000235:genetics*; D009569:Nitric Oxide / Q000502:physiology; D018384:Oxidative Stress / Q000502:physiology; D016159:Tumor Suppressor Protein p53 / Q000502:physiology*
chemical_list: D016159:Tumor Suppressor Protein p53; D009569:Nitric Oxide