The P53 Gene And Cancer Answers - Fill Online, Printable 2025

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In most cases, the p53 gene is mutated, giving rise to a stable mutant protein whose accumulation is regarded as a hallmark of cancer cells. Mutant p53 proteins not only lose their tumor suppressive activities but often gain additional oncogenic functions that endow cells with growth and survival advantages.
The p53 gene like the Rb gene, is a tumor suppressor gene, i.e., its activity stops the formation of tumors. If a person inherits only one functional copy of the p53 gene from their parents, they are predisposed to cancer and usually develop several independent tumors in a variety of tissues in early adulthood.
Role of a p53 gene? The TP53 gene provides instructions for making a protein called tumor protein p53 (or p53). This protein acts as a tumor suppressor, which means that it regulates cell division by keeping cells from growing and dividing (proliferating) too fast or in an uncontrolled way.

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Cell-cycle arrest and apoptosis are the most prominent outcomes of p53 activation. Many studies showed that p53 cell-cycle and apoptosis functions are important for preventing tumor development. p53 also regulates many cellular processes including metabolism, antioxidant response, and DNA repair.
p53 is a tumor suppressor protein that regulates the cell cycle and thus functions as a tumor suppressor that is involved in preventing cancer. Activated p53 binds to the G1-S/CDK (CDK2) and S/CDK complexes (molecules important for the G1/S transition in the cell cycle) inhibiting their activity.
P53 allows the cells with the repaired DNA to continue to divide. If the damaged cells are beyond repair then p53 will trigger the destruction of the cell. If the p53 protein is abnormal it will fail to stop the cell division and repair of a cell that has damaged DNA. This allows the damaged cell to continue to divide.
However, in its best described role as a guardian of the genome, p53 plays a central role in regulating the response to DNA-damage by balancing the activation of cell-cycle arrest and DNA-damage repair to promote cell survival versus activating apoptosis and cell death [12].
These mutations result in an altered p53 protein that cannot regulate cell proliferation effectively and is unable to trigger apoptosis in cells with mutated or damaged DNA. As a result, DNA damage can accumulate in cells. Such cells may continue to divide in an uncontrolled way, leading to the growth of tumors.

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Cancer and the Cell Cycle

Over half of all sporadic (random, non-hereditary) cancers have a mutation in the P53 gene. Why do you think a mutation in the p53 gene leads to so many cancers

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