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p53 pathway: In a normal cell, p53 is inactivated by its negative regulator, mdm2. Upon DNA damage or other stresses, various pathways will lead to the dissociation of the p53 and mdm2 complex. Once activated, p53 will induce a cell cycle arrest to allow either repair and survival of the cell or apoptosis to discard the damaged cell.
When there is too much damage, apoptosis is triggered in order to protect the organism from potentially harmful cells.7 p53, also known as a tumor suppressor gene, is a major regulatory protein in the DNA damage response system which binds directly to the promoters of its target genes. p53 acts primarily at the G1 checkpoint (controlling the G1 ...
The addition of agents such as Herceptin, Iressa, or Gleevec works to stop cells from cycling and causes apoptosis activation by blocking growth and survival signaling further upstream. Finally, adding p53-MDM2 complexes displaces p53 and activates the p53 pathway, leading to cell cycle arrest and apoptosis. Many different methods can be used ...
Many cancers exhibit mutations in the p53 gene, but this mutation can only be detected through extensive DNA sequencing. Studies have shown that cells with p53 mutations have significantly lower levels of PUMA, making it a good candidate for a protein marker of p53 mutations, providing a simpler method for testing for p53 mutations. [44]
This is known as cell cycle arrest. [12] This function of TIGAR forms part of the p53 mediated DNA damage response where, under low levels of cellular stress, p53 initiates cell cycle arrest to allow the cell time for repair. [13] [17] [18] Under high levels of cellular stress, p53 initiates apoptosis instead. [13] [17] [18]
P53 causes cells to enter apoptosis and disrupt further cell division therefore preventing that cell from becoming cancerous (16). In the majority of cancers it is the p53 pathway that has become mutated resulting in lack of ability to terminate dysfunctional cells.
The enlarged cells that are able to re-enter the cell cycle are prone to DNA damage and experience abnormalities in signaling for repair (NHEJ pathway), eventually leading to a replication failure and a permanent cell-cycle exit. [24] Overall, a consistent correlation between larger cell size and senescence has been established.
Absence of p53, the most commonly mutated gene in human cancer, has a major effect on cell cycle checkpoint regulators and has been shown to act at the G1 checkpoint in the past, but now appears to be important in regulating the spindle checkpoint as well. [76] Another key aspect of cancer is inhibition of cell death or apoptosis.