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

1.6K
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...
1.6K
Cancer Prevention02:59

Cancer Prevention

7.2K
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...
7.2K
Criteria for Causality: Bradford Hill Criteria - II01:28

Criteria for Causality: Bradford Hill Criteria - II

869
The Bradford Hill criteria serve as guidelines for establishing causative links in epidemiological research. Beyond Strength, Consistency, Specificity, and Temporality, key criteria also include Biological Gradient, Plausibility, Coherence, Experiment, and Analogy. These principles assist scientists in assessing the likelihood of causation in complex biological contexts. Below is a summary of these concepts:
869
Types of Toxins01:36

Types of Toxins

2.8K
Humans continually engage with an environment rich in potentially harmful chemicals. These are introduced to our bodies through inhalation, ingestion, or skin contact. These chemicals exist in various forms, such as air and environmental pollutants, agricultural chemicals, organic solvents, and heavy metals.
Air pollutants, primarily gases, pose significant threats to respiratory health, leading to conditions like hypoxia, lung cancer, and in extreme cases, death.
Environmental pollutants like...
2.8K
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

9.6K
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...
9.6K
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

8.5K
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...
8.5K

You might also read

Related Articles

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

Sort by
Same author

The crucible of resilience: hormesis as the unifying principle of evolution, genetics, and epigenetics.

Archives of toxicology·2026
Same author

Hormesis in biomedical and toxicological models: A generalizable phenomenon induced by per- and polyfluoroalkyl agents.

Chemico-biological interactions·2026
Same author

Canine environmental health: An EPA blind spot? Canine physiology, environmental exposure, and the regulatory gap in U.S. policy.

Regulatory toxicology and pharmacology : RTP·2026
Same author

Hormetic effects of per- and polyfluoroalkyl substances on ecologically relevant animal models: Generality, quantitative features, and risk assessment implications.

Environmental pollution (Barking, Essex : 1987)·2026
Same author

How the US NAS BEAR I Genetics Panel scientific misconduct could have been avoided, but was not.

Journal of occupational and environmental hygiene·2026
Same author

BEAR I Genetics Panel: An unexpected and troubling historical twist: The untold story of Hermann Muller's significant scientific confusion.

Journal of occupational and environmental hygiene·2026

Related Experiment Video

Updated: Nov 10, 2025

High Content Screening Analysis to Evaluate the Toxicological Effects of Harmful and Potentially Harmful Constituents HPHC
11:38

High Content Screening Analysis to Evaluate the Toxicological Effects of Harmful and Potentially Harmful Constituents HPHC

Published on: May 10, 2016

12.5K

Thresholds for carcinogens.

Edward J Calabrese1, Nicholas D Priest2, Walter J Kozumbo3

  • 1Department of Environmental Health Sciences, Morrill I, N344, University of Massachusetts, Amherst, MA, 01003, USA.

Chemico-Biological Interactions
|April 6, 2021
PubMed
Summary

Cancer risk assessment may need updating. Tumor latency, not just incidence, suggests carcinogen thresholds exist, challenging the linear no-threshold model for low-dose exposures.

Keywords:
Cancer risk assessmentHormesisLinear no-threshold (LNT)Nrf2Tumor latencyTumor promotion

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

14.9K
Formation of Covalent DNA Adducts by Enzymatically Activated Carcinogens and Drugs In Vitro and Their Determination by 32P-postlabeling
09:33

Formation of Covalent DNA Adducts by Enzymatically Activated Carcinogens and Drugs In Vitro and Their Determination by 32P-postlabeling

Published on: March 20, 2018

14.0K

Related Experiment Videos

Last Updated: Nov 10, 2025

High Content Screening Analysis to Evaluate the Toxicological Effects of Harmful and Potentially Harmful Constituents HPHC
11:38

High Content Screening Analysis to Evaluate the Toxicological Effects of Harmful and Potentially Harmful Constituents HPHC

Published on: May 10, 2016

12.5K
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

14.9K
Formation of Covalent DNA Adducts by Enzymatically Activated Carcinogens and Drugs In Vitro and Their Determination by 32P-postlabeling
09:33

Formation of Covalent DNA Adducts by Enzymatically Activated Carcinogens and Drugs In Vitro and Their Determination by 32P-postlabeling

Published on: March 20, 2018

14.0K

Area of Science:

  • Toxicology
  • Carcinogenesis
  • Risk Assessment

Background:

  • Current cancer risk assessment relies on the linear no-threshold (LNT) model, extrapolating high-dose rodent bioassay data to predict low-dose human cancer risks.
  • The LNT model assumes a linear dose-response relationship, estimating cancer risk based on tumor incidence.

Purpose of the Study:

  • To re-evaluate tumor latency as an alternative method for estimating carcinogen-induced cancer risks at low doses.
  • To examine the relationship between tumor latency, dose, dose rates, and key concepts in carcinogenesis.

Main Methods:

  • Integrated toxicological analysis of existing experimental evidence.
  • Examination of tumor latency (time-to-tumor) in relation to carcinogen dose and dose rates.
  • Discussion of concepts including tumor promotion, initiation, and hormesis.

Main Results:

  • Tumor latency is inversely related to carcinogen dose.
  • Evidence suggests quantifiable latency thresholds below which tumor promotion and progression are delayed or prevented.
  • These findings align with thresholds for tumor incidence and hormesis.

Conclusions:

  • Rethinking the linear no-threshold model's foundational premises is warranted.
  • Carcinogen thresholds, supported by tumor latency data, should be incorporated into updated cancer risk assessment practices.
  • This approach offers theoretical, experimental, and mechanistic support for revising current methodologies.