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-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

9.1K
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...
9.1K
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

12.5K
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...
12.5K
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

5.1K
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...
5.1K
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

7.9K
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...
7.9K
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

5.9K
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,...
5.9K
Mutagenicity and Carcinogenicity01:25

Mutagenicity and Carcinogenicity

1.4K
Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...
1.4K

You might also read

Related Articles

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

Sort by
Same author

The structural basis of RanGAP1 regulation and catalysis in nuclear transport.

bioRxiv : the preprint server for biology·2026
Same author

ERK autoinhibition mechanism informs a drug combination strategy.

Protein science : a publication of the Protein Society·2026
Same author

How Functional Variants Reconfigure the Rac2 Conformational Landscape.

bioRxiv : the preprint server for biology·2026
Same author

Energy landscapes in molecular biology: History, principles, and perspectives.

Quarterly reviews of biophysics·2026
Same author

Cyclin-E/A/CDK1/2 Kinetic Landscapes Drive Cell Cycle Phase-Specific Progression and Guide Cyclin-E Degradation Strategy.

Journal of chemical information and modeling·2026
Same author

Oncogenic PI3Kα variants reveal graded conformational spectrum with mutation-specific cryptic pockets.

Communications chemistry·2026

Related Experiment Video

Updated: Aug 29, 2025

Comparative Lesions Analysis Through a Targeted Sequencing Approach
08:16

Comparative Lesions Analysis Through a Targeted Sequencing Approach

Published on: November 5, 2019

6.8K

A New View of Activating Mutations in Cancer.

Ruth Nussinov1,2, Chung-Jung Tsai1, Hyunbum Jang1

  • 1Computational Structural Biology Section, Frederick National Laboratory for Cancer Research in the Cancer Innovation Laboratory, NCI, Frederick, Maryland.

Cancer Research
|September 7, 2022
PubMed
Summary
This summary is machine-generated.

Cancer development may depend more on signaling strength than activating mutations. Understanding these signal thresholds is key to improving patient outcomes for cancer and other diseases.

More Related Videos

Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors
11:15

Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors

Published on: September 20, 2016

24.5K
Deciphering the Structural Effects of Activating EGFR Somatic Mutations with Molecular Dynamics Simulation
15:05

Deciphering the Structural Effects of Activating EGFR Somatic Mutations with Molecular Dynamics Simulation

Published on: May 20, 2020

8.7K

Related Experiment Videos

Last Updated: Aug 29, 2025

Comparative Lesions Analysis Through a Targeted Sequencing Approach
08:16

Comparative Lesions Analysis Through a Targeted Sequencing Approach

Published on: November 5, 2019

6.8K
Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors
11:15

Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors

Published on: September 20, 2016

24.5K
Deciphering the Structural Effects of Activating EGFR Somatic Mutations with Molecular Dynamics Simulation
15:05

Deciphering the Structural Effects of Activating EGFR Somatic Mutations with Molecular Dynamics Simulation

Published on: May 20, 2020

8.7K

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Extensive research has focused on identifying cancer driver mutations.
  • Recent findings challenge the primacy of activating mutations in tumor development, suggesting signal strength is more critical.

Purpose of the Study:

  • To investigate the role of signaling strength versus activating mutations in cancer development.
  • To explore factors influencing signaling strength and its impact on cell fate.

Main Methods:

  • Analysis of factors affecting signal transduction pathways.
  • Examination of chromatin structure's role in regulating signal levels.
  • Correlation of signal strength with cellular processes like proliferation and senescence.

Main Results:

  • Signal strength, not the initiating mutation, appears to determine cell fate in tumorigenesis.
  • Factors such as homeostatic mechanisms, co-occurring mutations, and gene/protein expression levels modulate signaling strength.
  • Signal strength influences cell proliferation, oncogene-induced senescence, and is implicated in neurodevelopmental and neurodegenerative diseases.

Conclusions:

  • Cell fate and disease development are primarily dictated by signaling pathway strength.
  • Predicting and determining critical signaling thresholds are essential for therapeutic advancements in cancer and other conditions.