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Related Concept Videos

Mutagenicity and Carcinogenicity01:25

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

Cancer-Critical Genes I: Proto-oncogenes

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

Cancer-Critical Genes I: Proto-oncogenes

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...
Cancer Prevention02:59

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...
Skin Cancer01:30

Skin Cancer

Skin cancer is a type of cancer that occurs when there is an abnormal growth of skin cells, usually triggered by damage to the DNA within the skin cells. It is primarily caused by exposure to ultraviolet (UV) radiation from the sun or artificial sources like tanning beds. Skin cancer is the most common type of cancer worldwide, and its incidence continues to rise.
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Cancers Originate from Somatic Mutations in a Single Cell02:21

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...

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Related Experiment Video

Updated: Jun 2, 2026

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

An exposure driven functional model of carcinogenesis.

Eiliv Lund1

  • 1Institute of Community Medicine, University of Tromsø, 9037 Tromsø, Norway. eiliv.lund@uit.no

Medical Hypotheses
|May 10, 2011
PubMed
Summary

A new exposure-driven model proposes that carcinogens cause functional gene changes, leading to diverse cancer types. Stopping exposure may reverse cancer, offering new research and prevention strategies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epidemiology

Background:

  • Current cancer models focus on mutations as primary drivers.
  • Advances in molecular biology, genetics, and epidemiology offer new insights.
  • Existing models struggle to generate testable hypotheses for carcinogenesis.

Purpose of the Study:

  • Introduce and elaborate on the exposure-driven functional model of carcinogenesis.
  • Highlight the potential of this model to explain diverse cancer phenotypes.
  • Propose requirements for testing hypotheses within this novel framework.

Main Methods:

  • Integrates epidemiological findings with basic research.
  • Leverages emerging transcriptomics and epigenetics technologies.
  • Emphasizes the need for valid exposure measurements and robust study designs.

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

Published on: March 20, 2018

Related Experiment Videos

Last Updated: Jun 2, 2026

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

Modeling Oral-Esophageal Squamous Cell Carcinoma in 3D Organoids
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Modeling Oral-Esophageal Squamous Cell Carcinoma in 3D Organoids

Published on: December 23, 2022

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

Main Results:

  • Proposes that exposures, not mutations, are the primary determinants of carcinogenesis.
  • Suggests that diverse exposures and functional changes lead to varied cancer phenotypes.
  • Hypothesizes that exposure cessation can halt or reverse the carcinogenic process.

Conclusions:

  • The exposure-driven functional model offers a new paradigm for understanding cancer.
  • This model facilitates hypothesis testing regarding specific exposures and their effects.
  • Functional genomics and systems epidemiology are crucial for validating this model and improving cancer causality assessment.