Regulation of tissue- and stimulus-specific cell fate decisions by p53 in vivo.
The tumour suppressor p53 pathway is often inactivated by multiple mechanisms in the genesis of human cancers. Aberrant cellular proliferation, DNA damage, hypoxia, and ribosomal stress cause activation of the p53 tumour suppressor with multiple possible consequences to the cell: cell death, cell cycle arrest, or senescence. These mechanisms ultimately ensure that the cell does not replicate, and are thus potent tumour suppressor mechanisms. An important question that has eluded the field is how p53 makes these cell fate decisions. This review summarizes the current status of knowledge regarding p53-mediated stress and tissue-dependent cell fate decisions in mouse models and human tumours.
Jackson
James G
JG
Department of Genetics, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Post
Sean M
SM
Lozano
Guillermina
G
D000818:Animals; D017209:Apoptosis / Q000235:genetics; D002453:Cell Cycle / Q000235:genetics; D016922:Cellular Senescence / Q000235:genetics; D016158:Genes, p53; D006801:Humans; D051379:Mice; D009369:Neoplasms / Q000235:genetics* / Q000473:pathology; D009374:Neoplasms, Experimental / Q000235:genetics / Q000473:pathology; D011832:Radiation Injuries / Q000235:genetics / Q000473:pathology; D016159:Tumor Suppressor Protein p53 / Q000502:physiology*
D016159:Tumor Suppressor Protein p53