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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]
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]
WRAP53 (also known as WD40-encoding RNA antisense to p53) is a gene implicated in cancer development. The name was coined in 2009 to describe the dual role of this gene, encoding both an antisense RNA that regulates the p53 tumor suppressor and a protein involved in DNA repair, telomere elongation and maintenance of nuclear organelles Cajal bodies (Figure 1).
The phase of the cell cycle at which the blockage occurs primarily depends on the p53 protein. In cells containing the so-called "wild type" (non-mutated) p53, the cell cycle is halted in the interphase, while in cells with mutated p53, it is halted in the G 2 /M phase. [44] [50] Mechanism of action of arsenic trioxide. [51]
Most cases of lung cancer are because of genetic mutations in EGFR, KRAS, STK11 (also known as LKB1), TP53 (also known as p53), and CDKN2A (also known as p16 or INK4a) [117] [118] [119] with the most common type of lung cancer being an inactivation at p16. p16 is a tumor suppressor protein that occurs in mostly in humans the functional ...
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]
Indirect gene therapy. One of the challenges of cancer treatment is how to destroy malignant tumors without damaging healthy cells. A new method that shows great promise for accomplishing this employs the use of a suicide gene. A suicide gene is a gene which will cause a cell to kill itself through apoptosis.
Like p53, p73 is characterized by the presence of different isoforms of the protein. This is explained by splice variants, and an alternative promoter in the DNA sequence. p73, also known as tumor protein 73 (TP73), protein was the first identified homologue of the tumor suppressor gene, p53. Like p53, p73 has several variants.