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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...
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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

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Interactions Between Signaling Pathways01:19

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

Published on: August 4, 2019

Pathologies associated with the p53 response.

Andrei V Gudkov1, Elena A Komarova

  • 1Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, New York 14263, USA. andrei.gudkov@roswellpark.org

Cold Spring Harbor Perspectives in Biology
|July 3, 2010
PubMed
Summary
This summary is machine-generated.

The tumor suppressor p53, while crucial for cancer prevention, can cause severe pathologies under extreme stress. Temporarily suppressing p53 may reduce damage in conditions like radiation toxicity and ischemic diseases.

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Identifying DNA Mutations in Purified Hematopoietic Stem/Progenitor Cells
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Published on: February 24, 2014

Area of Science:

  • Molecular biology
  • Oncology
  • Pathology

Background:

  • The p53 protein is a critical tumor suppressor, preventing cancer by regulating cell responses to stress.
  • However, under extreme stress conditions, p53 can paradoxically induce severe pathologies, including treatment toxicities and acute ischemic diseases.

Purpose of the Study:

  • To investigate the dual role of p53 in disease pathogenesis.
  • To explore the therapeutic potential of transient p53 suppression in mitigating p53-associated pathologies.

Main Methods:

  • Analysis of animal models subjected to ionizing radiation and DNA damaging agents.
  • Examination of tissue-specific p53 responses, including apoptosis and cell cycle arrest.
  • Review of experimental data on p53's role in acute ischemic diseases.

Main Results:

  • p53 is a major contributor to the toxicity of ionizing radiation and chemotherapy, particularly affecting the hematopoietic system.
  • p53-induced damage is tissue-specific, leading to apoptosis in sensitive tissues (e.g., hematopoietic system) but promoting survival via cell cycle arrest in others (e.g., intestinal endothelium).
  • Evidence suggests p53 contributes to the pathology of acute ischemic conditions.

Conclusions:

  • Transient, reversible suppression of p53 using small molecules presents a promising and safe strategy to reduce the severity of various p53-associated pathologies.
  • Targeting p53 activity offers a novel therapeutic avenue for managing treatment side effects and ischemic diseases.