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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 ]
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]
P53 diverged from p63/p73 with a gene duplication in the cartilaginous fish. [7] P63 and p73 differentiated from each other in bony fish. [ 7 ] In vertebrates, p53 began the role of protecting the somatic cells and acting as a tumor suppressor.
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 ...
Tumor suppressor p53-binding protein 1 also known as p53-binding protein 1 or 53BP1 is a protein that in humans is encoded by the TP53BP1 gene. [ 5 ] [ 6 ] [ 7 ] Clinical significance
Mutated p53 is also involved in the pathophysiology of leukemias, lymphomas, sarcomas, and neurogenic tumors. Abnormalities of the p53 gene can be inherited in Li-Fraumeni syndrome (LFS), which increases the risk of developing various types of cancers. BCL2. BCL2 is a family of proteins that are involved in either inducing or inhibiting ...
P53, a transcription factor, can bind two sites within the human TIGAR gene to activate expression. [9] [13] One site is found within the first intron, and binds p53 with high affinity. [9] [13] The second is found just prior to the first exon, binds p53 with low affinity, [9] [13] and is conserved between mice and humans. [9]
Suicide genes must be introduced into the cells in ways that ensure their uptake and expression by as many cancer cells as possible, while limiting their expression by normal cells. Suicide gene therapy for cancer requires the vector to have the capacity to discriminate between target and non target cells, between the cancer cells and normal cells.