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 Stem Cells and Tumor Maintenance02:40

Cancer Stem Cells and Tumor Maintenance

4.9K
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...
4.9K
Metastasis02:30

Metastasis

5.5K
Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
5.5K
Cancer Prevention02:59

Cancer Prevention

6.1K
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...
6.1K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

3.8K
The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
3.8K

You might also read

Related Articles

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

Sort by
Same author

Mechanics-driven emergence of mesenchymal migration features.

Biomechanics and modeling in mechanobiology·2026
Same author

Beyond the Warburg Effect: Modeling the Dynamic and Context-Dependent Nature of Tumor Metabolism.

Cancers·2025
Same author

On the Importance of Acidity in Cancer Cells and Therapy.

Biology·2024
Same author

Characterization of the Intracellular Acidity Regulation of Brain Tumor Cells and Consequences for Therapeutic Optimization of Temozolomide.

Biology·2023
Same author

Generalization of the Ratiometric Method to Extend pH Range Measurements of the BCECF Probe.

Biomolecules·2023
Same author

Searching for the Metabolic Signature of Cancer: A Review from Warburg's Time to Now.

Biomolecules·2022
Same journal

RETRACTED: Sabir et al. DNA Based and Stimuli-Responsive Smart Nanocarrier for Diagnosis and Treatment of Cancer: Applications and Challenges. <i>Cancers</i> 2021, <i>13</i>, 3396.

Cancers·2026
Same journal

Correction: Adeluola et al. Chemoprevention of 4-NQO-Induced Oral Cancer by the Combination of Resveratrol and EGCG: In Vivo, In Silico and In Vitro Studies. <i>Cancers</i> 2026, <i>18</i>, 1098.

Cancers·2026
Same journal

Correction: Peñalver et al. Guidelines for Diagnosis, Treatment, and Follow-Up of Patients with Follicular Lymphoma-Spanish Lymphoma Group (GELTAMO) 2026. <i>Cancers</i> 2026, <i>18</i>, 395.

Cancers·2026
Same journal

Correction: Accorsi Buttini et al. Development of a Simplified Geriatric Score-4 (SGS-4) to Predict Outcomes After Allogeneic Hematopoietic Stem Cell Transplantation in Patients Aged over 50. <i>Cancers</i> 2025, <i>17</i>, 3278.

Cancers·2026
Same journal

Age-Stratified Long-Term Outcomes of Immune Checkpoint Inhibitors for Stage IV Melanoma and NSCLC in The Netherlands: A Population-Based Study.

Cancers·2026
Same journal

Targeting Ferroptosis in Glioblastoma: Molecular Mechanisms, Tumor Microenvironment, and Therapeutic Opportunities.

Cancers·2026
See all related articles

Related Experiment Video

Updated: Jun 21, 2025

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

2.3K

Is Cancer Metabolism an Atavism?

Eric Fanchon1, Angélique Stéphanou1

  • 1Université Grenoble Alpes, CNRS, UMR 5525, VetAgro Sup, Grenoble INP, TIMC, 38000 Grenoble, France.

Cancers
|July 13, 2024
PubMed
Summary
This summary is machine-generated.

Cancer metabolism does not fully align with the Serial Atavism Model (SAM). While cancer cells exhibit ancient traits, their diverse metabolic states challenge the idea of a simple reversion to ancestral types.

Keywords:
Warburg effectcancer theorygene expressionhypoxiametabolic plasticity

More Related Videos

Extraction of Aqueous Metabolites from Cultured Adherent Cells for Metabolomic Analysis by Capillary Electrophoresis-Mass Spectrometry
11:39

Extraction of Aqueous Metabolites from Cultured Adherent Cells for Metabolomic Analysis by Capillary Electrophoresis-Mass Spectrometry

Published on: June 9, 2019

9.1K
Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy
07:20

Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy

Published on: January 31, 2025

429

Related Experiment Videos

Last Updated: Jun 21, 2025

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

2.3K
Extraction of Aqueous Metabolites from Cultured Adherent Cells for Metabolomic Analysis by Capillary Electrophoresis-Mass Spectrometry
11:39

Extraction of Aqueous Metabolites from Cultured Adherent Cells for Metabolomic Analysis by Capillary Electrophoresis-Mass Spectrometry

Published on: June 9, 2019

9.1K
Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy
07:20

Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy

Published on: January 31, 2025

429

Area of Science:

  • Evolutionary biology
  • Cancer research
  • Metabolic pathways

Background:

  • The atavistic theory suggests cancer involves reverting to ancestral cellular phenotypes.
  • The Serial Atavism Model (SAM) proposes cancer progression through multiple atavistic reversions.
  • The Warburg effect, a key feature of SAM, links cancer metabolism to ancient cellular states.

Purpose of the Study:

  • To evaluate if cancer metabolism represents an atavistic reversion.
  • To analyze cancer metabolism characteristics within the SAM framework.

Main Methods:

  • Review of existing literature on cancer metabolism.
  • Analysis of known cancer hallmarks and metabolic states.
  • Interrogation of the SAM's applicability to cancer metabolism.

Main Results:

  • Cancer metabolism exhibits a wide spectrum of states.
  • These diverse metabolic states are not adequately explained by a sequential reversion to an ancient state.
  • The atavistic theory, as framed by SAM, may not fully capture cancer metabolism's complexity.

Conclusions:

  • Cancer metabolism is too complex to be solely explained by the Serial Atavism Model.
  • The atavistic theory needs refinement to adequately frame cancer research.
  • Further investigation into the nature of cancer metabolism is warranted.