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The TP53 gene is the most frequently mutated gene (>50%) in human cancer, indicating that the TP53 gene plays a crucial role in preventing cancer formation. [5] TP53 gene encodes proteins that bind to DNA and regulate gene expression to prevent mutations of the genome. [12]
TP53 is the most frequently mutated gene (>50%) in human cancer, suggesting that it has a key role in preventing cancer formation. [13] The cellular mechanisms and transcriptional programs involved in p53 activation are complicated. There is evidence that p53 can suppress tumors, but it can also can cause toxicity in normal tissues.
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]
The hope is that future research into TIGAR will provide insight into new ways to treat cancer. [ 8 ] [ 9 ] [ 10 ] This gene is regulated as part of the p53 tumor suppressor pathway and encodes a protein with sequence similarity to the bisphosphate domain of the glycolytic enzyme that degrades fructose-2,6-bisphosphate.
One of the most significant tumor suppressors is known as p53. It plays such a critical role in regulation of cell division and cell death that in 70% of cancer cells p53 is found either mutated or functionally inactivated. Often times tumors can not form successfully without deactivating critical tumor suppressors like p53. [6]
The p53 protein was discovered 10 years earlier by several groups, including that of David Lane and Lionel Crawford, Arnold Levine, and Lloyd Old. But there was no evidence that p53 played a major role in human cancers, and the gene encoding p53 (TP53) was thought to be an oncogene rather than a tumor suppressor gene.
The p53 p63 p73 family is a family of tumor suppressor genes. [1] [2] This gene family codes the proteins: p53; TP73L (also known as "p63") p73; They are sometimes considered part of a "p53 family." When overexpressed, these proteins are known to be involved in tumor pathogenesis. [3]
Levine received his Ph.D. from the University of Pennsylvania in 1966. [3]Levine discovered, with several colleagues, the p53 tumor suppressor gene in 1979, a protein involved in cell cycle regulation, and one of the most frequently mutated genes in human cancer, in work done as a professor in the biochemistry department at Princeton University.