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Related Concept Videos

Replicative Cell Senescence02:15

Replicative Cell Senescence

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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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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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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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Cancer Stem Cells and Tumor Maintenance02:40

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Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
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DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart,...
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Related Experiment Video

Updated: Sep 19, 2025

Generation of Cancer Cell Clones to Visualize Telomeric Repeat-containing RNA TERRA Expressed from a Single Telomere in Living Cells
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Telomeres and Cancer: Resolving the Paradox.

Joe Nassour1, Tobias T Schmidt1, Jan Karlseder1

  • 1Molecular and Cell Biology Laboratory, The Salk Institute for Biological Studies, La Jolla, California 92037, USA.

Annual Review of Cancer Biology
|September 17, 2021
PubMed
Summary
This summary is machine-generated.

Telomeres, chromosome ends, protect against cancer by triggering DNA damage signals. However, they also drive cancer mutations like chromothripsis, presenting a dual role in tumorigenesis.

Keywords:
genome instabilityproliferative life span barriersreplicative crisisreplicative senescencetelomeretumorigenesis

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

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Area of Science:

  • Genetics
  • Cell Biology
  • Cancer Research

Background:

  • Cell cycle regulation governs cellular lifespan and is often dysregulated in cancer.
  • Telomeres, chromosome ends, act as critical barriers to cellular proliferation and tumor growth.
  • Telomere dysfunction initiates DNA damage responses, impacting cell cycle, inflammation, and cell death.

Purpose of the Study:

  • To review the dual role of telomeres in cancer development.
  • To explore how telomeres contribute to genomic instability in tumors.
  • To reconcile the paradoxical functions of telomeres in carcinogenesis.

Main Methods:

  • Literature review of decades of research on telomere biology and cancer.
  • Analysis of recent findings on telomere-mediated genomic aberrations, including chromothripsis.
  • Synthesis of current knowledge on telomere's tumor-suppressive and tumor-promoting functions.

Main Results:

  • Telomeres act as tumor suppressors by initiating DNA damage responses.
  • Telomeres are a significant source of genomic aberrations in cancer, such as chromothripsis.
  • Telomere shortening exhibits a dual effect, potentially promoting or inhibiting cancer progression.

Conclusions:

  • Telomeres possess a paradoxical role in cancer etiology, acting as both suppressors and drivers.
  • Understanding telomere's dual function is crucial for reconciling their implications in cancer.
  • Further research is needed to fully elucidate the complex relationship between telomeres and cancer.