Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
Replicative Cell Senescence02:15

Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...
Replicative Cell Senescence02:15

Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Direct probabilistic quantification of mosaic loss of chromosome Y from sequencing data.

bioRxiv : the preprint server for biology·2026
Same author

An Essential Role for Senescent Cells in Optimal Wound Healing through Secretion of PDGF-AA.

Developmental cell·2026
Same author

How long can humans live? All evidence points to a maximum of 125 years.

Nature·2026
Same author

Mutagen-induced somatic mutation rate in primary mammalian cells in relation to maximum life span.

Geromedicine·2026
Same author

The aging genome exhibits organized vulnerability to somatic mutations.

bioRxiv : the preprint server for biology·2026
Same author

Evidence for negative selection against somatic mutations induced in normal fibroblasts by <i>N</i>-ethyl-<i>N</i>-nitrosourea.

Genome research·2026

Related Experiment Video

Updated: Jun 24, 2026

Combining Magnetic Sorting of Mother Cells and Fluctuation Tests to Analyze Genome Instability During Mitotic Cell Aging in Saccharomyces cerevisiae
11:08

Combining Magnetic Sorting of Mother Cells and Fluctuation Tests to Analyze Genome Instability During Mitotic Cell Aging in Saccharomyces cerevisiae

Published on: October 16, 2014

Genome instability, cancer and aging.

Alexander Y Maslov1, Jan Vijg

  • 1Department of Genetics, Albert Einstein College of Medicine, Bronx, NY 10461, USA. amaslov@aecom.yu.edu

Biochimica Et Biophysica Acta
|April 7, 2009
PubMed
Summary

Genome instability from DNA damage drives evolution but harms individuals. Age-related mutations and epimutations increase cancer risk and organ decline, impacting stem cells.

Area of Science:

  • Genetics
  • Cell Biology
  • Aging Research

Background:

  • DNA damage is crucial for evolution but harmful to somatic cells.
  • Cellular responses include cell death, cell cycle arrest, and DNA repair.
  • Errors in DNA repair and chromatin restoration lead to age-related mutations and epimutations.

Purpose of the Study:

  • To review age-related changes in the mammalian genome.
  • To explore the functional consequences of these changes.
  • To emphasize genome instability in stem/progenitor cells.

Main Methods:

  • Literature review of age-related genomic changes.
  • Analysis of DNA damage response pathways.
  • Focus on stem/progenitor cell genome instability.

More Related Videos

Evaluating the Effect of SASP Factors on the Proliferation of Cancer Cells Using a Comparative Analysis of Three Distinct Methodologies
08:57

Evaluating the Effect of SASP Factors on the Proliferation of Cancer Cells Using a Comparative Analysis of Three Distinct Methodologies

Published on: September 19, 2025

Studying Age-dependent Genomic Instability using the S. cerevisiae Chronological Lifespan Model
08:46

Studying Age-dependent Genomic Instability using the S. cerevisiae Chronological Lifespan Model

Published on: September 29, 2011

Related Experiment Videos

Last Updated: Jun 24, 2026

Combining Magnetic Sorting of Mother Cells and Fluctuation Tests to Analyze Genome Instability During Mitotic Cell Aging in Saccharomyces cerevisiae
11:08

Combining Magnetic Sorting of Mother Cells and Fluctuation Tests to Analyze Genome Instability During Mitotic Cell Aging in Saccharomyces cerevisiae

Published on: October 16, 2014

Evaluating the Effect of SASP Factors on the Proliferation of Cancer Cells Using a Comparative Analysis of Three Distinct Methodologies
08:57

Evaluating the Effect of SASP Factors on the Proliferation of Cancer Cells Using a Comparative Analysis of Three Distinct Methodologies

Published on: September 19, 2025

Studying Age-dependent Genomic Instability using the S. cerevisiae Chronological Lifespan Model
08:46

Studying Age-dependent Genomic Instability using the S. cerevisiae Chronological Lifespan Model

Published on: September 29, 2011

Main Results:

  • Accumulation of mutations and epimutations with age.
  • Increased cancer risk and impaired organ function in aged tissues.
  • Potential common mechanisms driving cellular degeneration and proliferation in aging.

Conclusions:

  • Age-related genome instability, particularly in stem cells, contributes to aging.
  • Understanding these changes is key to addressing age-related diseases.
  • Genome maintenance is critical for mitigating aging effects.