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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]
Even though PUMA function is compromised in most cancer cells, it does not appear that genetic inactivation of PUMA is a direct target of cancer. [ 36 ] [ 37 ] [ 38 ] Many cancers do exhibit p53 gene mutations, making gene therapies that target this gene [ clarification needed ] impossible, but an alternate pathway may be to focus on ...
Several drug therapies are being developed based on p53, the tumour suppressor gene that protects the cell in response to damage and stress. It is analogous to deciding what to do with a damaged car: p53 brings everything to a halt, and then decides whether to fix the cell or, if the cell is beyond repair, to destroy the cell.
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.
TP-53 is a gene that encodes for the protein p53; this protein is a tumor suppressor. p53 was discovered in 1979 stemming from a study involving cancer immunology and the role of viruses in some cancers. The protein was so named because it was measured to have a weight of 53 kDa.
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 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]
Gendicine enters the tumour cells by way of receptor-mediated endocytosis and begins to over-express genes coding for the p53 protein needed to fight the tumour. [3] Ad-p53 seems to act by stimulating the apoptotic pathway in tumour cells, which increases the expression of tumour suppressor genes and immune response factors (such as the ability of natural killer (NK) cells to exert "bystander ...