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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...
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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...
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: Jun 26, 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

p53 polymorphisms: cancer implications.

Catherine Whibley1, Paul D P Pharoah, Monica Hollstein

  • 1Leeds Institute of Genetics, Health and Therapeutics, LIGHT Laboratories, University of Leeds, Leeds, LS2 9JT, UK.

Nature Reviews. Cancer
|January 24, 2009
PubMed
Summary
This summary is machine-generated.

TP53 gene mutations are common in cancer, impairing p53 tumor suppression. This review examines TP53 single nucleotide polymorphisms (SNPs) and their potential cancer-related effects, including interactions with MDM2 variants.

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Last Updated: Jun 26, 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

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence
04:56

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence

Published on: December 30, 2025

Area of Science:

  • Genetics
  • Cancer Biology
  • Molecular Oncology

Background:

  • The p53 protein is a critical tumor suppressor, and its normal function is essential for preventing cancer development.
  • Mutations in the TP53 gene are frequently observed in human tumors, leading to significant loss of p53 function.
  • In contrast to cancer-causing mutations, naturally occurring TP53 single nucleotide polymorphisms (SNPs) are generally thought to have minimal impact on p53 function.

Purpose of the Study:

  • To review the TP53 gene locus polymorphisms and their potential to influence cancer-related phenotypes.
  • To discuss polymorphic variants in the p53 pathway, such as MDM2, and their potential biological consequences, individually or in combination with TP53 variants.

Main Methods:

  • Literature review of TP53 gene variations and their functional consequences.
  • Analysis of existing data on single nucleotide polymorphisms (SNPs) within the TP53 gene.
  • Examination of studies investigating the role of MDM2 polymorphisms in cancer.

Main Results:

  • While TP53 mutations are hallmarks of cancer, most TP53 SNPs are unlikely to cause significant functional defects in p53.
  • Certain TP53 polymorphisms may have subtle effects on p53 function, potentially influencing cancer risk or phenotype.
  • Polymorphisms in interacting genes, like MDM2, can modify the biological impact of TP53 variants.

Conclusions:

  • The functional impact of TP53 polymorphisms on cancer is an area requiring further investigation.
  • Understanding the interplay between TP53 variants, SNPs, and other pathway components like MDM2 is crucial for a comprehensive view of cancer biology.
  • This review highlights the importance of considering genetic variations beyond canonical mutations in the context of cancer etiology and progression.