Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Epigenetic Regulation

Epigenetic Regulation

Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.

Cancers Originate from Somatic Mutations in a Single Cell

Cancers Originate from Somatic Mutations in a Single Cell

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...

Cancer Prevention

Cancer Prevention

Several factors can increase the risk of cancer in an individual. About 50% of cancer cases can be prevented by adopting a healthy lifestyle, regular exercise, eating healthy, and following a modest cancer prevention diet. Epidemiological studies have consistently shown that populations with vegetable and fruit-rich diets have reduced the incidence of cancer. On the other hand, populations who have a diet rich in animal fat, red meat, junk food, or high calories are predisposed to cancer.
Some...

Epigenetic Regulation

Epigenetic Regulation

Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...

Cancers Originate from Somatic Mutations in a Single Cell

Cancers Originate from Somatic Mutations in a Single Cell

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...

Mutagenicity and Carcinogenicity

Mutagenicity and Carcinogenicity

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...

You might also read

Related Articles

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

Sort by

Same author

Targeted degradation of MDM2 overcomes feedback regulation of p53 signaling in Merkel cell carcinoma models.

The Journal of clinical investigation·2026

Same author

ESR1 mutations and CDK4/6 inhibitor choice shape clonal selection and adaptive cell states during acquired resistance.

Genome medicine·2026

Same author

A pan-cancer single-cell analysis of intratumoral copy number diversity and evolution.

Cancer discovery·2026

Same author

H3K27M-driven hypertranscription leads to a new targetable dependency in diffuse midline gliomas.

bioRxiv : the preprint server for biology·2026

Same author

Radiation Oncology-Biology Integration Network: Bridging the Gap between Biological Research and Clinical Practice.

Clinical cancer research : an official journal of the American Association for Cancer Research·2026

Same author

HER2 heterogeneous breast cancer models reveal novel therapeutic targets and subclonal dynamics during evolution to resistance to HER2-targeted therapies.

Cancer discovery·2026

Search research articles

Related Experiment Video

Updated: Jul 29, 2026

Rapid Analysis of Chromosome Aberrations in Mouse B Lymphocytes by PNA-FISH

Rapid Analysis of Chromosome Aberrations in Mouse B Lymphocytes by PNA-FISH

Published on: August 19, 2014

Chromosomal instability and human cancer.

Franziska Michor¹

¹Program for Evolutionary Dynamics, Department of Organismic and Evolutionary Biology, Harvard University, Cambridge MA 02138, USA. michor@fas.harvard.edu

Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences

|May 18, 2005

Summary

Chromosomal instability (CIN) drives cancer development by increasing genetic mutations during cell division. Mathematical models reveal CIN as a causal factor in human tumorigenesis, impacting cancer genetics.

More Related Videos

Generation and Isolation of Cell Cycle-arrested Cells with Complex Karyotypes

Generation and Isolation of Cell Cycle-arrested Cells with Complex Karyotypes

Published on: April 13, 2018

Long-term Live-cell Imaging to Assess Cell Fate in Response to Paclitaxel

Long-term Live-cell Imaging to Assess Cell Fate in Response to Paclitaxel

Published on: May 14, 2018

Related Experiment Videos

Last Updated: Jul 29, 2026

Rapid Analysis of Chromosome Aberrations in Mouse B Lymphocytes by PNA-FISH

Rapid Analysis of Chromosome Aberrations in Mouse B Lymphocytes by PNA-FISH

Published on: August 19, 2014

Generation and Isolation of Cell Cycle-arrested Cells with Complex Karyotypes

Generation and Isolation of Cell Cycle-arrested Cells with Complex Karyotypes

Published on: April 13, 2018

Long-term Live-cell Imaging to Assess Cell Fate in Response to Paclitaxel

Long-term Live-cell Imaging to Assess Cell Fate in Response to Paclitaxel

Published on: May 14, 2018

Area of Science:

Genetics
Cancer Biology
Mathematical Biology

Background:

Genetic instability, particularly chromosomal instability (CIN), is a hallmark of human cancers.
CIN involves an elevated rate of gross chromosomal alterations during cell division.
Mutations in CIN genes, which maintain genomic integrity, cause CIN.

Purpose of the Study:

To investigate the causal relationship between chromosomal instability (CIN) and human cancer development.
To explore whether genetic instability acts as a driving force in tumorigenesis.

Main Methods:

Utilized a mathematical framework to model the somatic evolution of cancer.
Analyzed the role of CIN in the context of cancer genetics.

Main Results:

The study provides insights into the causal links between CIN and human cancer.
Mathematical modeling supports the role of CIN in driving tumorigenesis.

Conclusions:

Chromosomal instability is a significant factor in the development of human cancer.
Genetic instability, specifically CIN, is a causal element in the initiation and progression of cancer.