Contained in chromosome 17p.

TP53, tumor protein 53 is one of the most frequent altered identifiable genes in cancer.

Encodes for the P53 protein, which plays a role in anti-proliferation of a number of target genes.

In normal cells p53 induces growth arrest and apoptosis when DNA damage occurs.

TP53 known as the guardian of the genome, as you can mount a potent defense against cancers.

Tumor suppressor gene-most common mutated gene in human solid tumors.

The prevalence of pathogenic germline variants of TP 53 may be as high as 0.2% in the general population.

Loss of tumor suppressor p53 gene often results in genomic instability, which could lead to the aneuploidy genotype.

It is a transcription factor that inhibits cell division or survival in response to stresses.

Germline mutations in TP53 increases the risk for multiple cancers and is associated with the Li-Fraumeni syndrome.

Two copies of the P 53 gene are present in every cell and if one copy and undergoes a mutation it results in a mixture of normal and mutant versions of the P53 protein.

A nuclear phosphoprotein that suppresses uncontrolled cell division.

A normal p53 function prevents malignant transformation.

Has a critical role in many pathways that prevent cancer, such as repairing DNA or killing cells if they have irreparable DNA damage.

Estimated to be mutated in approximately 50% of malignancies.

In certain circumstances can be an oncogene.

p53, after genotoxic stress, can trigger cellular senescence, apoptosis or cell cycle arrest.

Lack of functional p53 molecules impairs cellular processes so that cells escape apoptosis, proliferate, accumulate other DNA abnormalities, disease progression and chemoresistance.

Less than 1% of cancers associated with TP53 mutation.

Mutations result in reduced drug sensitivity.

Tumor suppressor gene has significant role in balance of cell proliferation and apoptosis in cell response to stress.

Suppresses lung carcinogenesis (Robles).

Mutations result in structural changes that enable the mutant gene to become more stable and allows its accumulation (Wiethege T).

TP53 alterations is associated with high risk of treatment resistance and failure in childhood ALL (Hof J et al).

Almost all types of NSCLC express p53 mutation, which leads to genomic instability and gain of function properties.

P53 mutations are responsible for nearly half of ovarian cancers; 43 percent of colorectal cancers; 38 percent of lung cancers; nearly one-third of pancreatic, stomach, and liver cancers; and one-quarter of breast cancers, among others.

Radiation should be avoided in patients who have breast cancer with germline TP53 mutations because these mutations increase the chance of radiation-induced cancers, including angiosarcoma.

P 53 mutations associated with a higher risk of peripheral artery disease.

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