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Related Concept Videos

Overview of DNA Repair02:25

Overview of DNA Repair

In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
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Abnormal Proliferation02:23

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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...
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
Overview of DNA Repair02:25

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In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
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Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...

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Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis
12:55

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Published on: February 16, 2015

Apoptosis and genomic instability.

Boris Zhivotovsky1, Guido Kroemer

  • 1Institute of Environmental Medicine, Karolinska Institutet, Box 210, Nobels väg 13, SE-171 77 Stockholm, Sweden. boris.zhivotovsky@imm.ki.se

Nature Reviews. Molecular Cell Biology
|September 2, 2004
PubMed
Summary
This summary is machine-generated.

Genomic instability and apoptosis are closely connected, impacting cancer development. Altered apoptosis pathways contribute to genomic instability, while DNA repair proteins influence apoptosis, highlighting their critical roles in cancer pathophysiology.

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Last Updated: May 30, 2026

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Published on: February 16, 2015

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Area of Science:

  • Genetics
  • Cell Biology
  • Oncology

Background:

  • Genomic instability is a hallmark of cancer.
  • Apoptosis, or programmed cell death, is a crucial mechanism for eliminating damaged cells.
  • Dysregulation of apoptosis contributes to cancer development and progression.

Purpose of the Study:

  • To elucidate the intricate relationship between genomic instability and apoptosis.
  • To understand how alterations in apoptosis control contribute to cancer pathophysiology.
  • To explore the role of DNA repair proteins in regulating apoptosis.

Main Methods:

  • Review of existing literature on genomic instability and apoptosis.
  • Analysis of molecular mechanisms linking DNA damage response and apoptotic pathways.
  • Examination of cancer genomics data for correlations between instability and apoptosis markers.

Main Results:

  • Genomic instability, including chromosomal and microsatellite instability, can lead to the inactivation of pro-apoptotic pathways.
  • Inhibition of apoptosis allows survival of cells with unrepaired DNA damage, telomere dysfunction, or polyploidy.
  • DNA repair proteins have been identified as regulators of apoptosis.

Conclusions:

  • Genomic instability and apoptosis are intimately linked phenomena.
  • The interplay between genomic instability and apoptosis has significant implications for cancer development.
  • Targeting these pathways holds potential for cancer therapy.