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

Mutagenicity and Carcinogenicity01:25

Mutagenicity and Carcinogenicity

1.9K
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...
1.9K
Mismatch Repair01:20

Mismatch Repair

6.3K
Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
6.3K
Mismatch Repair01:36

Mismatch Repair

43.5K
Overview
43.5K
Spontaneous and Induced Mutations01:30

Spontaneous and Induced Mutations

2.0K
Spontaneous mutations arise infrequently during DNA replication due to errors in the process. A key factor behind these errors is tautomeric shifts in nitrogenous bases, where bases transition from keto to enol forms or amino to imino forms. This shift can alter base-pairing rules, leading to mutations. Additionally, reactive oxygen species (ROS) arising from aerobic metabolism can damage DNA, resulting in depurination (loss of a purine base) or depyrimidination (loss of a pyrimidine base).
2.0K
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

6.9K
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,...
6.9K
Mouse Models of Cancer Study02:43

Mouse Models of Cancer Study

6.4K
Mice have long served as models for studying human biology and pathology because of their phylogenetic and physiological similarity with humans. They are also easy to maintain and breed in the laboratory, and hence, many inbred strains are now available for research. Studies on mice have contributed immeasurably to our understanding of cancer biology.
The development of transgenic, knockout, and knock-in mice has led to an exponential increase in their use as model organisms in research,...
6.4K

You might also read

Related Articles

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

Sort by
Same author

Biological sex influences severity and outcomes in <i>Acinetobacter baumannii</i> pneumonia.

Microbiology spectrum·2025
Same author

Secrets of the Stratum Corneum I: Parakeratosis or Porokeratosis?

Skinmed·2025
Same author

Editors and Journals: Part III-"<i>Sto Tavo</i> (Who Is In Charge)?"

Skinmed·2024
Same author

Multiple Eruptive Dermatofibromas in Systemic Lupus Erythematosus.

Skinmed·2024
Same author

Guiding the future of clinical care and clinical research in Birt-Hogg-Dubé.

European journal of human genetics : EJHG·2024
Same author

Dermatology One Hundred Years Ago.

Skinmed·2024
Same journal

Spatial Heterogeneity of Phytoplankton Taxa and Functional Groups Under Multidimensional Environmental Factors in Karst Urban Rivers.

Biology·2026
Same journal

Paleopathology of a Lower Miocene Carettochelyid Turtle from the Moghra Formation, Egypt.

Biology·2026
Same journal

Effects of Type I Diabetes Mellitus and Masticatory Loading on Mandibular Growth in Growing Rats: A Longitudinal CBCT Study.

Biology·2026
Same journal

Data-Limited Stock Status Assessment of Bonga Shad, <i>Ethmalosa fimbriata</i> (Bowdich, 1825) and Lesser African Threadfin, <i>Galeoides decadactylus</i> (Bloch, 1795) in the Central Gulf of Guinea.

Biology·2026
Same journal

Gonadogenesis in the Bearded Dragon (<i>Pogona vitticeps</i>, Agamidae): A Comprehensive Histological Analysis from Gonadal Ridge Formation to Testicular and Ovarian Development.

Biology·2026
Same journal

The Programmable Microbiome: Integrative AI and Multi-Omics Frameworks for Precision T2DM Management.

Biology·2026
See all related articles

Related Experiment Video

Updated: Jan 13, 2026

The Lambda Select cII Mutation Detection System
07:08

The Lambda Select cII Mutation Detection System

Published on: April 26, 2018

8.3K

Carcinogenesis: An Alternative Hypothesis Comparing Mutagenic Versus Metabolic Models.

Albert Alhatem1, Claude E Gagna1,2, Muriel W Lambert1

  • 1Departments of Pathology and Dermatology, Rutgers-New Jersey Medical School, Newark, NJ 07103, USA.

Biology
|October 29, 2025
PubMed
Summary
This summary is machine-generated.

Metabolic reprogramming, not just genetic mutations, may initiate cancer. Cancer cells

Keywords:
Warburg effectangiogenesisatavistic responsecarcinogenesiscell migrationmetabolic reprogrammingmutationsoxidative phosphorylation

More Related Videos

Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate DMBA-TPA
04:12

Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate DMBA-TPA

Published on: December 19, 2019

15.2K
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

3.1K

Related Experiment Videos

Last Updated: Jan 13, 2026

The Lambda Select cII Mutation Detection System
07:08

The Lambda Select cII Mutation Detection System

Published on: April 26, 2018

8.3K
Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate DMBA-TPA
04:12

Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate DMBA-TPA

Published on: December 19, 2019

15.2K
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

3.1K

Area of Science:

  • Oncology
  • Metabolic pathways
  • Cellular metabolism

Background:

  • Carcinogenesis is traditionally linked to genetic mutations affecting cell proliferation and apoptosis.
  • The Warburg effect, observed in cancer cells, shows a preference for glycolysis over oxidative phosphorylation, suggesting metabolic dysregulation's role.
  • Metabolic dysregulation may be a primary driver of neoplastic transformation.

Purpose of the Study:

  • To explore carcinogenesis as a consequence of metabolic reprogramming.
  • To investigate the hypothesis that cellular energy loss triggers atavistic responses driving cancer.
  • To bridge the gap between genetic and metabolic pathways in carcinogenesis.

Main Methods:

  • This study is primarily theoretical, based on existing research and the Warburg effect.
  • It proposes a hypothesis linking metabolic dysregulation to cancer initiation.
  • The proposed mechanism involves cellular energy loss stimulating atavistic responses.

Main Results:

  • Metabolic dysregulation, particularly energy loss, may instigate neoplastic transformation.
  • Atavistic responses, including rapid proliferation and migration, are triggered by energy deficits.
  • These responses contribute to pathological angiogenesis and uncontrolled cell growth.

Conclusions:

  • Metabolic reprogramming is a significant factor in carcinogenesis, potentially preceding genetic mutations.
  • Cellular energy status plays a crucial role in initiating cancer development.
  • Understanding metabolic pathways offers new perspectives on cancer's genetic and metabolic links.