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Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...

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Related Experiment Video

Updated: May 30, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

TP53-Associated Pediatric Malignancies.

Emilia M Pinto1, Raul C Ribeiro, Bonald C Figueiredo

  • 1International Outreach Program, St. Jude Children's Research Hospital, Memphis, TN, USA.

Genes & Cancer
|July 23, 2011
PubMed
Summary

Germline TP53 mutations are linked to childhood cancers. Different inherited TP53 alleles influence cancer risk, with adrenocortical carcinoma serving as a model for TP53 inactivation effects.

Keywords:
Arg337Hisadrenocortical tumorsp53 mutation

Related Experiment Videos

Last Updated: May 30, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

Area of Science:

  • Oncology
  • Genetics
  • Pediatric Medicine

Background:

  • The TP53 tumor suppressor pathway is crucial in preventing cancer.
  • While most childhood cancers have wild-type p53, inherited TP53 mutations are significant contributors.
  • Germline TP53 mutations lead to Li-Fraumeni syndrome and increase susceptibility to various cancers.

Purpose of the Study:

  • To review childhood cancers associated with TP53 functional inactivation.
  • To highlight the role of inherited mutant TP53 alleles in cancer risk.
  • To use adrenocortical carcinoma as a model for TP53-sensitive tissues.

Main Methods:

  • Literature review of epidemiological and genetic studies on TP53 and childhood cancer.
  • Analysis of TP53 mutation data in pediatric malignancies.
  • Case study focus on adrenocortical carcinoma in the context of TP53 inactivation.

Main Results:

  • Epidemiological data show diverse inherited TP53 alleles with varying tumor suppressor activity.
  • These alleles correlate with cancer risk, including penetrance, age of onset, and specific tumor types.
  • Adrenocortical carcinoma exemplifies tissues highly sensitive to the loss of p53 activity.

Conclusions:

  • Functional inactivation of the TP53 pathway is a key factor in specific pediatric cancers.
  • Understanding inherited TP53 variations is critical for assessing childhood cancer risk.
  • Further research into TP53-sensitive tissues can elucidate cancer development mechanisms.