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Related Concept Videos

Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
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...
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...
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...
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...
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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DNA-Damage-Induced Alternative Splicing of p53.

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Related Experiment Video

Updated: Jul 6, 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

Wild-type p53: tumors can't stand it.

Michael B Kastan1

  • 1Department of Oncology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA. michael.kastan@stjude.org

Cell
|March 14, 2007
PubMed
Summary

Restoring tumor suppressor p53 function can trigger cancer regression in mice. However, tumors may develop resistance by bypassing the p53 pathway.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Malignant tumors frequently disrupt the p53 signaling pathway for growth and survival.
  • The p53 pathway is a critical regulator of cell cycle arrest, apoptosis, and DNA repair.
  • Mutations in p53 are common in various human cancers.

Purpose of the Study:

  • To investigate the therapeutic potential of restoring p53 function in cancer treatment.
  • To evaluate whether p53 restoration alone is sufficient for tumor regression.
  • To identify potential mechanisms of tumor resistance to p53-based therapies.

Main Methods:

  • Studies involved restoring p53 function in mouse models of different tumor types.
  • Researchers analyzed tumor regression following p53 pathway reactivation.

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

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Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells
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Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

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Published on: December 30, 2025

  • Mechanisms of acquired resistance were investigated in subsequent experiments.

    • Main Results:

    • Restoration of p53 function led to the regression of several types of tumors in mice.
    • These findings suggest p53 reactivation as a potential cancer therapy.
    • Tumors demonstrated the ability to rapidly develop resistance by circumventing the p53 pathway.

    Conclusions:

    • Restoring p53 activity shows promise as a potent anti-cancer strategy.
    • Tumor resistance mechanisms can emerge quickly, posing a therapeutic challenge.
    • Further research is needed to overcome resistance and develop effective p53-based cancer treatments.