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

Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

5.7K
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,...
5.7K
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

11.9K
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...
11.9K
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

8.8K
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...
8.8K
Tumor Progression02:07

Tumor Progression

6.3K
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...
6.3K
Mechanisms of Retrovirus-induced Cancers01:51

Mechanisms of Retrovirus-induced Cancers

5.1K
Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...
5.1K
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

7.4K
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...
7.4K

You might also read

Related Articles

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

Sort by
Same author

Constraints on the G1/S transition pathway may favor selection of multicellularity as a passenger phenotype.

eLife·2026
Same author

Immunological surveillance against cancer across mammals.

Nature communications·2025
Same author

Advancing cancer research via comparative oncology.

Nature reviews. Cancer·2025
Same author

Purine Biosynthesis Pathways Are Required for Myogenesis in <i>Xenopus laevis</i>.

Cells·2023
Same author

Reuniting philosophy and science to advance cancer research.

Biological reviews of the Cambridge Philosophical Society·2023
Same author

Immunological exhaustion: How to make a disparate concept operational?

PLoS pathogens·2021

Related Experiment Video

Updated: Jun 28, 2025

A Protocol for Genetic Induction and Visualization of Benign and Invasive Tumors in Cephalic Complexes of Drosophila melanogaster
07:23

A Protocol for Genetic Induction and Visualization of Benign and Invasive Tumors in Cephalic Complexes of Drosophila melanogaster

Published on: September 11, 2013

9.6K

Critically assessing atavism, an evolution-centered and deterministic hypothesis on cancer.

Bertrand Daignan-Fornier1, Thomas Pradeu2,3

  • 1University of Bordeaux, CNRS, IBGC, Bordeaux, France.

Bioessays : News and Reviews in Molecular, Cellular and Developmental Biology
|April 22, 2024
PubMed
Summary
This summary is machine-generated.

Cancer may stem from ancient, re-expressed genes from unicellular ancestors, according to the atavism hypothesis. This evolutionary perspective offers new insights into cancer development and control mechanisms.

More Related Videos

Author Spotlight: Transmitochondrial Cybrid Generation Using Cancer Cell Lines
07:49

Author Spotlight: Transmitochondrial Cybrid Generation Using Cancer Cell Lines

Published on: March 17, 2023

2.4K
Generation of Heterogeneous Drug Gradients Across Cancer Populations on a Microfluidic Evolution Accelerator for Real-Time Observation
10:24

Generation of Heterogeneous Drug Gradients Across Cancer Populations on a Microfluidic Evolution Accelerator for Real-Time Observation

Published on: September 19, 2019

6.4K

Related Experiment Videos

Last Updated: Jun 28, 2025

A Protocol for Genetic Induction and Visualization of Benign and Invasive Tumors in Cephalic Complexes of Drosophila melanogaster
07:23

A Protocol for Genetic Induction and Visualization of Benign and Invasive Tumors in Cephalic Complexes of Drosophila melanogaster

Published on: September 11, 2013

9.6K
Author Spotlight: Transmitochondrial Cybrid Generation Using Cancer Cell Lines
07:49

Author Spotlight: Transmitochondrial Cybrid Generation Using Cancer Cell Lines

Published on: March 17, 2023

2.4K
Generation of Heterogeneous Drug Gradients Across Cancer Populations on a Microfluidic Evolution Accelerator for Real-Time Observation
10:24

Generation of Heterogeneous Drug Gradients Across Cancer Populations on a Microfluidic Evolution Accelerator for Real-Time Observation

Published on: September 19, 2019

6.4K

Area of Science:

  • Evolutionary biology
  • Cancer research
  • Genetics

Background:

  • Cancer is often attributed to somatic mutations driving uncontrolled cell growth and invasion.
  • Some theories suggest cancer arises from a breakdown in multicellularity, releasing cells from normal controls.
  • The evolutionary framework offers novel perspectives on cancer's origins.

Purpose of the Study:

  • To critically review the atavism hypothesis of cancer.
  • To explore the evolutionary perspective of cancer as a re-emergence of ancestral traits.
  • To identify areas needing clarification within the atavism hypothesis.

Main Methods:

  • Literature review and critical analysis of the atavism hypothesis.
  • Examination of evolutionary transitions in multicellularity.
  • Comparative genomics and developmental biology perspectives.

Main Results:

  • The atavism hypothesis proposes cancer involves re-expression of ancestral gene programs.
  • This perspective links cancer to the evolution of multicellularity and gene regulation.
  • The hypothesis offers a unique evolutionary viewpoint on cancer's underlying mechanisms.

Conclusions:

  • The atavism hypothesis provides a valuable evolutionary lens for understanding cancer.
  • Further clarification and unification of the hypothesis's features are needed.
  • Integrating evolutionary insights could advance cancer research and therapeutic strategies.