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

Cancer Stem Cells and Tumor Maintenance02:40

Cancer Stem Cells and Tumor Maintenance

5.2K
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.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
5.2K
Tumor Progression02:07

Tumor Progression

6.7K
Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
6.7K
Replicative Cell Senescence02:15

Replicative Cell Senescence

4.0K
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...
4.0K
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

5.3K
Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
5.3K
Tumor Immunotherapy01:27

Tumor Immunotherapy

790
Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.
790
Treatment Resistant Cancers02:56

Treatment Resistant Cancers

3.5K
Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
3.5K

You might also read

Related Articles

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

Sort by
Same author

FXR-YAP signalling maintains biliary epithelial cell identity and preserves liver homeostasis.

Nature metabolism·2026
Same author

Glutamate as a therapeutic strategy to promote liver regeneration.

Clinical and translational medicine·2025
Same author

p53 protein degradation redefines the initiation mechanisms and drives transitional mutations in colorectal cancer.

Nature communications·2025
Same author

Macrophages harness hepatocyte glutamate to boost liver regeneration.

Nature·2025
Same author

Endogenous retroviruses shape pluripotency specification in mouse embryos.

Science advances·2024
Same author

Transit-amplifying cells control R-spondins in the mouse crypt to modulate intestinal stem cell proliferation.

The Journal of experimental medicine·2022

Related Experiment Video

Updated: Nov 2, 2025

An In Vitro System to Study Tumor Dormancy and the Switch to Metastatic Growth
09:14

An In Vitro System to Study Tumor Dormancy and the Switch to Metastatic Growth

Published on: August 11, 2011

16.0K

When dormancy fuels tumour relapse.

Karla Santos-de-Frutos1, Nabil Djouder2

  • 1Molecular Oncology Programme, Growth Factors, Nutrients and Cancer Group, Centro Nacional de Investigaciones Oncológicas (CNIO), Madrid, Spain.

Communications Biology
|June 17, 2021
PubMed
Summary

Dormant cancer cells, including quiescent and senescent types, can persist after treatment and cause tumour relapse. Understanding their distinct roles is crucial for improving cancer therapies and preventing recurrence.

More Related Videos

An In Vitro Dormancy Model of Estrogen-sensitive Breast Cancer in the Bone Marrow: A Tool for Molecular Mechanism Studies and Hypothesis Generation
08:48

An In Vitro Dormancy Model of Estrogen-sensitive Breast Cancer in the Bone Marrow: A Tool for Molecular Mechanism Studies and Hypothesis Generation

Published on: June 30, 2015

8.4K
A Time-lapse, Label-free, Quantitative Phase Imaging Study of Dormant and Active Human Cancer Cells
12:48

A Time-lapse, Label-free, Quantitative Phase Imaging Study of Dormant and Active Human Cancer Cells

Published on: February 16, 2018

7.6K

Related Experiment Videos

Last Updated: Nov 2, 2025

An In Vitro System to Study Tumor Dormancy and the Switch to Metastatic Growth
09:14

An In Vitro System to Study Tumor Dormancy and the Switch to Metastatic Growth

Published on: August 11, 2011

16.0K
An In Vitro Dormancy Model of Estrogen-sensitive Breast Cancer in the Bone Marrow: A Tool for Molecular Mechanism Studies and Hypothesis Generation
08:48

An In Vitro Dormancy Model of Estrogen-sensitive Breast Cancer in the Bone Marrow: A Tool for Molecular Mechanism Studies and Hypothesis Generation

Published on: June 30, 2015

8.4K
A Time-lapse, Label-free, Quantitative Phase Imaging Study of Dormant and Active Human Cancer Cells
12:48

A Time-lapse, Label-free, Quantitative Phase Imaging Study of Dormant and Active Human Cancer Cells

Published on: February 16, 2018

7.6K

Area of Science:

  • Oncology
  • Cancer Biology
  • Cellular Senescence

Background:

  • Tumour recurrence is a significant challenge in cancer treatment.
  • Conventional therapies like chemotherapy and radiotherapy primarily target rapidly dividing cancer cells.
  • Non-proliferative dormant cancer cells can survive treatment, leading to relapse.

Purpose of the Study:

  • To review the mechanisms of tumour recurrence driven by dormant cancer cells.
  • To differentiate the roles of quiescent versus senescent cancer cells in relapse.
  • To highlight the need for understanding these distinct cell states for therapeutic strategies.

Main Methods:

  • Literature review of studies on cancer dormancy, quiescence, and senescence.
  • Analysis of cell cycle regulation, metabolic features, and microenvironment interactions.
  • Synthesis of current knowledge on dormant cancer cell biology and therapeutic implications.

Main Results:

  • Quiescent cells exhibit reversible growth arrest, allowing potential re-entry into the cell cycle.
  • Senescent cells are irreversibly arrested and may promote tumour growth via paracrine signaling.
  • Dormant cancer cells, encompassing both quiescent and senescent states, possess distinct characteristics influencing tumour relapse.

Conclusions:

  • Quiescent and senescent cancer cells have different but potentially complementary roles in tumour growth and relapse.
  • Understanding the specific contributions of each cell state is essential for developing effective anti-relapse strategies.
  • Targeting dormant cancer cells requires tailored approaches based on their unique biological properties.