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Mutagenicity and Carcinogenicity

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...

Spontaneous and Induced Mutations

Spontaneous and Induced Mutations

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).

Mismatch Repair

Mismatch Repair

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...

Mismatch Repair

Mismatch Repair

In-vitro Mutagenesis

In-vitro Mutagenesis

To learn more about the function of a gene, researchers can observe what happens when the gene is inactivated or “knocked out,” by creating genetically engineered knockout animals. Knockout mice have been particularly useful as models for human diseases such as cancer, Parkinson’s disease, and diabetes.

Mutations

Mutations

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Related Experiment Video

Updated: Feb 17, 2026

Production and Detection of Reactive Oxygen Species ROS in Cancers

Production and Detection of Reactive Oxygen Species ROS in Cancers

Published on: November 21, 2011

Inflammation, ROS, and Mutagenesis.

Asmaa El-Kenawi¹, Brian Ruffell²

¹Department of Immunology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA.

|December 13, 2017

Summary

This summary is machine-generated.

Reactive oxygen species (ROS) are linked to cancer. This study shows that increased ROS from myeloid cells alone can cause intestinal mutations, supporting their role in tumor development.

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Last Updated: Feb 17, 2026

Production and Detection of Reactive Oxygen Species ROS in Cancers

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Published on: November 21, 2011

Stimulation of Stem Cell Niches and Tissue Regeneration in Mouse Skin by Switchable Protoporphyrin IX-Dependent Photogeneration of Reactive Oxygen Species In Situ

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Studying Ribonucleotide Incorporation: Strand-specific Detection of Ribonucleotides in the Yeast Genome and Measuring Ribonucleotide-induced Mutagenesis

Studying Ribonucleotide Incorporation: Strand-specific Detection of Ribonucleotides in the Yeast Genome and Measuring Ribonucleotide-induced Mutagenesis

Published on: July 26, 2018

Area of Science:

Oncology
Immunology
Molecular Biology

Background:

Chronic inflammatory diseases are associated with higher cancer risk.
Reactive oxygen species (ROS) are suspected mediators of this link.
The specific cellular sources and mechanisms of ROS in tumorigenesis require further elucidation.

Purpose of the Study:

To investigate the role of myeloid cell-derived ROS in intestinal mutagenesis.
To determine if amplified ROS production by myeloid cells is sufficient to drive tumor development.

Main Methods:

Utilized mouse models to study ROS production in myeloid cells.
Employed genetic and pharmacological tools to manipulate ROS levels.
Assessed intestinal tissue for mutagenesis and tumor formation.

Main Results:

Amplified ROS production specifically in myeloid cells was sufficient to promote intestinal mutagenesis.
Myeloid cell-derived ROS directly contribute to DNA damage and mutations in the intestine.
Targeting ROS in myeloid cells may offer a therapeutic strategy.

Conclusions:

Myeloid cell-generated ROS are a key driver of intestinal mutagenesis.
This finding provides a mechanistic link between inflammation and cancer.
Further research into ROS-mediated pathways in myeloid cells is warranted for cancer prevention and treatment.