p53


Also found in: Dictionary, Acronyms, Encyclopedia, Wikipedia.

p53

A tumor suppressor gene located on the short arm of chromosome 17 that encodes a nucleophosphoprotein that binds DNA and negatively regulates cell division; frequently measured as a marker of malignant diseases.

p53

(pē′fĭf′tē-thrē′)
n.
1. A protein that regulates normal cell growth and proliferation and prevents unrestrained division of cells whose DNA has been damaged, as from ultraviolet or ionizing radiation. The absence of functional p53, usually resulting from a genetic mutation, increases the risk of developing various cancers.
2. The tumor suppressor gene that codes for this protein. Also called TP53.

p53

A 53 kD nuclear phosphoprotein encoded by the proto-oncogene p53, on chromosome 17p13; in its wild form, p53 inhibits cell growth control and transformation; it activates transcription of genes that suppress cell proliferation, acting as a tumor suppressor protein; if p53 is physically lost or functionally inactived, cells can grow without restraint. See Li-Fraumeni syndrome, p21, Tumor suppressor genes, WAF1.

p53

A tumor suppressor gene located on the short arm of chromosome 17 that encodes a nucleophosphoprotein that binds DNA and negatively regulates cell division; frequently measured as a marker of malignant diseases.

p53

A gene that codes for P21. A tumour suppressor gene, the absence or mutation of which can greatly increase the probability that cancer will develop. When DNA damage, as from anticancer drugs, occurs in normal cells the expression of p53 is increased. The p53 protein may then act to protect the cell by halting the cell cycle so that the DNA damage can be repaired, or, if the DNA damage is too severe, p53 protein can kill the cell by APOPTOSIS so that the defective DNA is not passed on. Mutations in p53 have been found in a range of cancers including those of the breast, colon, ovary, bladder and oesophagus. They have also been found to be associated with failure to respond to anticancer drugs.

p53

a tumor suppressor gene active in the cellular response to DNA damage and cell cycle arrest.
References in periodicals archive ?
Active P53 binds to target DNA and determines the choice between triggering cell cycle arrests at a checkpoint to allow DNA repair or activating a special molecular pathway leading to the self-destruction of a cell through apoptosis.
MDM2 Amplification, MIB-1, p53 and MDM2 Protein Expression Status, Cellularity, Neurofibromatosis Status, and Tumor Site in 15 Malignant Peripheral Nerve Sheath Tumors Case MDM2 to SE12 Ratio MIB-1 P53 MDM2 No.
In many tumors, the mutation lies in the portion of p53 called the DNA-binding domain.
ADVEXIN p53 therapy is a targeted molecular therapy with broad applicability in a wide range of tumor types and clinical settings because it targets one of the most fundamental and common molecular defects, abnormal p53 tumor suppressor function, associated with cancer initiation, progression and treatment resistance.
Objectives such as p53-dependent PFT-[alpha] regulation of hepatocyte proliferation in rats [19], the acceleration of cutaneous wound healing by the inhibitor through the inhibition of p53 function [20] and the protective role of the PFT-[alpha] in the inhibition of ischemic-reperfusion were addressed [21].
In multivariate analyses, patients who had abnormal p53 were 77% more likely to die from prostate cancer and 60% more likely to develop distant metastases at 5 years, compared with men without abnormal p53.
2 mM each of dATP, dCTP, dGTP, and dTTP (Eppendorf); 1 x p53 GeneChip primer set (Affymetrix); and 0.
The researchers suspect that too much p53 stunts the division of stem cells which normally replenish tissues such as skin and bones in adults.
When subjected to ultraviolet light, p53 in the defective cells was activated, prompting the researchers to surmise that another type of protein was involved.
Abnormal expression of the p53 gene was associated with both extrauterine spread of the disease and decreased 5-year, disease-free survival, said Dr.
Physicians at UCLA's Jonsson Comprehensive Cancer Center announced Thursday they are seeking 300 volunteers with ovarian cancer to participate in a new study of the genetic treatment, which targets mutations in a gene called p53.
One gene, for instance, produces a protein called p53 that works like a safety switch.