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Wenwei Hu
Assistant
Professor
UMDNJ-RWJMS
Dept. of Pediatrics
The Cancer Institute of New Jersey
195 Little Albany Street
New Brunswick. NJ 08903-2681
(732) 235-6169
FAX - 5331
huw1@umdnj.edu |
p53; tumor suppressor; stress response; apoptosis; single nucleotide
polymorphism; microRNA; tumor; development and reproduction
As "the guardian of the genome”, the p53 tumor suppressor gene plays a
critical role in maintaining genomic stability and tumor prevention. p53 is the
most frequently-mutated gene in human tumors; over 50% of all tumors harbor
mutations in the p53 gene, and over 80% of tumors have a dysfunctional p53
signaling pathway. The p53 protein responds to a wide variety of stress signals,
including DNA damage (e.g. IR and UV), hypoxia, mitotic spindle damage, the
inhibition of ribosome biogenesis, nutrition starvation and even the activation
of oncogenes or the inactivation of tumor suppressor genes. These stress signals
all interfere with the cellular homeostatic mechanisms that monitor and control
the fidelity of DNA replication, chromosome segregation and cell division. As a
transcription factor, once p53 is activated it selectively transcribes a set of
target genes to initiate various cellular responses. Depending upon the cell
type, and the type or degree of stress placed upon a cell, the p53 protein
induces cell cycle arrest, apoptosis or senescence, etc. to prevent the
propagation of cells that could potentially become cancerous.
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