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

Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

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...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

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...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

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.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

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.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

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.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...

You might also read

Related Articles

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

Sort by
Same author

EcDNA-borne structural variants drive oncogenic fusion transcript amplification.

Cellยท2026
Same author

Targeting the MYC oncogene with a selective bi-steric mTORC1 inhibitor elicits tumor regression in MYC-driven cancers.

Cell chemical biologyยท2025
Same author

EcDNA-borne PVT1 fusion stabilizes oncogenic mRNAs.

bioRxiv : the preprint server for biologyยท2025
Same author

Low-level shRNA Cytotoxicity Can Contribute to MYC-induced Hepatocellular Carcinoma in Adult Mice.

Molecular therapy : the journal of the American Society of Gene Therapyยท2025
Same author

Lactobacillus acidophilus potentiates oncolytic virotherapy through modulating gut microbiota homeostasis in hepatocellular carcinoma.

Nature communicationsยท2025
Same author

Spatial analysis reveals targetable macrophage-mediated mechanisms of immune evasion in hepatocellular carcinoma minimal residual disease.

Nature cancerยท2024

Related Experiment Video

Updated: Jun 29, 2026

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

Tumor dormancy and oncogene addiction.

Dean W Felsher1

  • 1Division of Oncology, Department of Medicine, Stanford University, Palo Alto, CA, USA. dfelsher@stanford.edu

APMIS : Acta Pathologica, Microbiologica, Et Immunologica Scandinavica
|October 7, 2008
PubMed
Summary

Targeting cancer-causing genes (oncogenes) can eliminate tumors through apoptosis, differentiation, or senescence. Understanding these mechanisms is key for effective cancer treatment strategies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Cancer arises from genetic alterations, including oncogene activation.
  • Targeting oncogenes shows promise in cancer therapy.
  • The precise outcomes of oncogene inactivation in tumors remain incompletely understood.

Purpose of the Study:

  • To investigate the diverse cellular responses to oncogene inactivation in cancer.
  • To elucidate the mechanisms driving tumor cell elimination, differentiation, senescence, or dormancy following oncogene inactivation.

Main Methods:

  • Utilized experimental transgenic mouse models.
  • Analyzed the genetic and cellular context influencing oncogene inactivation outcomes.

Main Results:

More Related Videos

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

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

Related Experiment Videos

Last Updated: Jun 29, 2026

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

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

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

  • Oncogene inactivation can lead to tumor cell apoptosis (oncogene addiction), terminal differentiation, or cellular senescence.
  • Some cells lose neoplastic properties but can regain them upon oncogene reactivation, leading to tumor dormancy.
  • Outcomes are highly dependent on the specific genetic and cellular environment.

Conclusions:

  • Oncogene inactivation triggers varied cellular fates, including cell death, differentiation, senescence, and dormancy.
  • Understanding these distinct responses is crucial for developing targeted cancer therapies.
  • Context-dependent outcomes highlight the complexity of oncogene-targeted cancer treatment.