TP53 and cancer: Nevertheless, theapparent cell- and damage-type specificity observed in post-translationalmodification signaling pathways highlights the need to develop tissue-specificexperimental cancer models that reflect the physiological switches that canactivate p53, including changes in cytokoines like transforming growth factorβ (TGF-β) or interferons, metabolic stresses like hypoxia, glucosestarvation or acidification, external stresses including carcinogen damage to DNA,and internal signals such as oncogene activation.