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

Replicative Cell Senescence02:15

Replicative Cell Senescence

3.5K
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...
3.5K
Replicative Cell Senescence02:15

Replicative Cell Senescence

3.0K
3.0K
Telomeres and Telomerase02:41

Telomeres and Telomerase

23.1K
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...
23.1K
Telomeres and Telomerase02:41

Telomeres and Telomerase

6.4K
6.4K
Replication in Eukaryotes01:29

Replication in Eukaryotes

15.4K
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.
Many Proteins Orchestrate Replication at the Origin
Eukaryotic replication follows many of the same...
15.4K
Replication in Eukaryotes02:31

Replication in Eukaryotes

156.9K
Overview
156.9K

You might also read

Related Articles

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

Sort by
Same author

Nur77 agonism invigorates Natural Killer cell immunity against hepatocellular carcinoma.

Nature communications·2026
Same author

Viruses and RQC: a molecular arms race at the heart of translation.

Trends in microbiology·2026
Same author

Albacarcin V adds EPLIN as a novel and promising target for the treatment of female cancers and pediatric medulloblastoma.

Biochemical pharmacology·2025
Same author

Transcriptomic profiles of endocrine-resistant breast cancer.

BMC cancer·2025
Same author

Differential regulation of translational stress responses by herpesvirus ubiquitin deconjugases.

The FEBS journal·2025
Same author

Computational pathology annotation enhances the resolution and interpretation of breast cancer spatial transcriptomics data.

NPJ precision oncology·2025

Related Experiment Video

Updated: May 3, 2026

Generation of Cancer Cell Clones to Visualize Telomeric Repeat-containing RNA TERRA Expressed from a Single Telomere in Living Cells
09:13

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

Published on: January 17, 2019

6.8K

Tumor viruses and replicative immortality--avoiding the telomere hurdle.

Xinsong Chen1, Siamak Akbari Kamranvar1, Maria G Masucci1

  • 1Department of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.

Seminars in Cancer Biology
|February 4, 2014
PubMed
Summary

Tumor viruses manipulate cell proliferation and telomere maintenance, often activating telomerase or Alternative Lengthening of Telomeres (ALT), to achieve long-term survival and malignancy. These viral strategies impact genomic stability during oncogenesis.

Keywords:
Alternative lengthening of telomereGenomic instabilityTelomeraseTelomereTumor virus

More Related Videos

Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer
08:34

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

Published on: April 13, 2015

13.3K
Ex Vivo Infection of Live Tissue with Oncolytic Viruses
12:08

Ex Vivo Infection of Live Tissue with Oncolytic Viruses

Published on: June 25, 2011

13.5K

Related Experiment Videos

Last Updated: May 3, 2026

Generation of Cancer Cell Clones to Visualize Telomeric Repeat-containing RNA TERRA Expressed from a Single Telomere in Living Cells
09:13

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

Published on: January 17, 2019

6.8K
Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer
08:34

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

Published on: April 13, 2015

13.3K
Ex Vivo Infection of Live Tissue with Oncolytic Viruses
12:08

Ex Vivo Infection of Live Tissue with Oncolytic Viruses

Published on: June 25, 2011

13.5K

Area of Science:

  • Oncology
  • Virology
  • Molecular Biology
  • Genetics

Background:

  • Tumor viruses induce cell proliferation for replication and persistence.
  • Viral oncogenesis involves growth transformation, often leading to telomere dysfunction and chromosome instability.
  • Bypassing senescence, triggered by damaged telomeres, is crucial for malignant progression.

Purpose of the Study:

  • To review strategies employed by tumor viruses to interfere with telomere homeostasis during cell transformation.
  • To highlight the role of telomere maintenance mechanisms in viral oncogenesis.

Main Methods:

  • Literature review of existing research on tumor viruses and telomere biology.
  • Analysis of mechanisms by which viruses affect telomere length and stability.
  • Examination of the interplay between viral products, cell cycle control, and telomere maintenance.

Main Results:

  • Tumor viruses frequently activate telomerase to maintain telomere integrity and function.
  • Oncogenic viruses may also activate the Alternative Lengthening of Telomeres (ALT) pathway.
  • Both telomerase activation and ALT contribute to bypassing senescence and enabling sustained proliferation.

Conclusions:

  • Tumor viruses utilize distinct strategies to manipulate telomere homeostasis, ensuring cellular immortality.
  • Activation of telomerase and ALT are key mechanisms enabling viral-driven cancer progression.
  • Understanding these viral strategies provides insights into cancer development and potential therapeutic targets.