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Related Concept Videos

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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...
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In eukaryotic DNA replication, a single-stranded DNA fragment remains at the end of a chromosome after the removal of the final primer. This section of DNA cannot be replicated in the same manner as the rest of the strand because there is no 3’ end to which the newly synthesized DNA can attach. This non-replicated fragment results in gradual loss of the chromosomal DNA during each cell duplication. Additionally, it can induce a DNA damage response by enzymes that recognize single-stranded...
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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...
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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.
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In eukaryotic cells, DNA replication is highly conserved and tightly regulated. Multiple linear chromosomes must be duplicated with high fidelity before cell division, so there are many proteins that fulfill specialized roles in the replication process. Replication occurs in three phases: initiation, elongation, and termination, and ends with two complete sets of chromosomes in the nucleus.
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Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
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Updated: Sep 11, 2025

Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer
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Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer

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Telomere Crisis Shapes Cancer Evolution.

Joe Nassour1, Jan Karlseder2

  • 1University of Colorado School of Medicine, Aurora, Colorado 80045, USA joe.nassour@cuanschutz.edu karlseder@salk.edu.

Cold Spring Harbor Perspectives in Biology
|August 11, 2025
PubMed
Summary
This summary is machine-generated.

Most mutations in normal cells don't cause cancer due to protective mechanisms like telomere crisis. This process suppresses tumors but can also drive cancer evolution in rare cases.

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

  • Oncology
  • Genetics
  • Cell Biology

Background:

  • Somatic mutations frequently occur in normal tissues, often affecting cancer-driver genes.
  • Despite mutations, most abnormal cell clones remain dormant, suggesting natural tumor suppression mechanisms exist.

Purpose of the Study:

  • To investigate the role of telomere crisis as a tumor-suppressive barrier.
  • To understand how telomere crisis influences the initiation and evolution of malignancy.

Main Methods:

  • Analysis of cellular responses to checkpoint defects and genomic instability.
  • Examination of the interplay between telomere crisis and tumor suppressor pathways (p53, pRb).

Main Results:

  • Telomere crisis acts as a potent barrier, eliminating cells with faulty checkpoints and evading surveillance.
  • Genomic instability during telomere crisis can promote clonal evolution, but cell death is the predominant outcome.
  • A rare fraction of cells escape telomere crisis to initiate malignancy.

Conclusions:

  • Telomere crisis is a critical, dual-acting mechanism in early cancer development.
  • Understanding telomere crisis is key to developing strategies against tumor-initiating cells.