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Updated: Jul 24, 2026

Telomere Length and Telomerase Activity; A Yin and Yang of Cell Senescence

Telomere Length and Telomerase Activity; A Yin and Yang of Cell Senescence

Published on: May 22, 2013

Telomeres, crisis and cancer.

R A Greenberg¹

¹Department of Cancer Biology, Dana Farber Cancer Institute, Boston, Massachusetts, USA. rgreenberg@partners.org

Current Molecular Medicine

|June 25, 2005

Summary

Telomere dysfunction triggers senescence, a tumor suppressor mechanism. However, bypassing senescence leads to crisis, accelerating chromosomal instability and potentially cancer development.

Area of Science:

Cell Biology
Genetics
Oncology

Background:

Eukaryotic chromosomes have specialized protein-DNA complexes called telomeres at their ends.
Telomere structure disruption activates DNA damage response pathways, leading to senescence.
Senescence acts as a tumor suppressor by limiting cell proliferation.

Purpose of the Study:

To review the relationship between telomere function during crisis and chromosomal instability.
To explore how telomere dysfunction contributes to cancer development.

Main Methods:

Review of existing literature on telomere biology, DNA damage response, senescence, and cancer.
Analysis of the role of telomeric crisis in genomic instability.

Main Results:

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Telomere Length and Telomerase Activity; A Yin and Yang of Cell Senescence

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Generation of Cancer Cell Clones to Visualize Telomeric Repeat-containing RNA TERRA Expressed from a Single Telomere in Living Cells

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Published on: January 17, 2019

Telomere dysfunction, if senescence is bypassed, leads to a state of crisis.
Crisis is characterized by cell death and significant chromosomal abnormalities.
This chromosomal instability is a hallmark of cancer and may promote neoplastic transformation.

Conclusions:

Telomere crisis accelerates chromosomal instability, a key factor in carcinogenesis.
Understanding telomere dynamics in crisis is crucial for cancer research.