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Related Concept Videos

Mutations in Microorganisms01:18

Mutations in Microorganisms

Mutations are heritable changes in an organism’s genome involving alterations in the base sequence of DNA or RNA. These changes can influence cellular processes and phenotypic traits, potentially transforming the unaltered wild type into a mutant form. Such changes, termed forward mutations, are pivotal in shaping the genetic diversity of organisms.RNA viruses exhibit the highest mutation rates due to the absence of robust proofreading mechanisms during genome replication. In contrast,...
Viral Mutations00:36

Viral Mutations

A mutation is a change in the sequence of bases of DNA or RNA in a genome. Some mutations occur during replication of the genome due to errors made by the polymerase enzymes that replicate DNA or RNA. Unlike DNA polymerase, RNA polymerase is prone to errors because it is not capable of “proofreading” its work. Viruses with RNA-based genomes, like HIV, therefore accrue mutations faster than viruses with DNA-based genomes. Because mutation and recombination provide the raw material for adaptive...
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...
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...
Mismatch Repair01:20

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 Repair01:36

Mismatch Repair

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Related Experiment Video

Updated: May 23, 2026

Measuring Microbial Mutation Rates with the Fluctuation Assay
07:44

Measuring Microbial Mutation Rates with the Fluctuation Assay

Published on: November 28, 2019

Infection, mutation, and cancer evolution.

Paul W Ewald1, Holly A Swain Ewald

  • 1Department of Biology, University of Louisville, Louisville, KY 40292, USA. pwewald@gmail.com

Journal of Molecular Medicine (Berlin, Germany)
|April 6, 2012
PubMed
Summary
This summary is machine-generated.

Integrating evolutionary insights with cancer mechanisms reveals infections and mutations as key drivers of oncogenesis. This perspective highlights the significant, often underestimated, role of infections in cancer development and evolution.

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Last Updated: May 23, 2026

Measuring Microbial Mutation Rates with the Fluctuation Assay
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Measuring Microbial Mutation Rates with the Fluctuation Assay

Published on: November 28, 2019

Transmitochondrial Cybrid Generation Using Cancer Cell Lines
07:49

Transmitochondrial Cybrid Generation Using Cancer Cell Lines

Published on: March 17, 2023

Area of Science:

  • Oncology
  • Evolutionary Biology
  • Infectious Disease

Background:

  • Understanding oncogenesis requires integrating mechanistic and evolutionary perspectives.
  • Infections and mutations are recognized as joint causes of many cancers.

Purpose of the Study:

  • To explore the broader causal role of infections in oncogenesis.
  • To explain the evolutionary pressures driving oncogenic mechanisms.

Main Methods:

  • Integration of mechanistic cancer studies with evolutionary theory.
  • Analysis of viral transmission routes and their selective pressures.

Main Results:

  • Infections may play a more significant role in oncogenesis than previously thought.
  • Oncogenic viruses often transmit via routes favoring host persistence (e.g., sexual, salivary contact).
  • Mechanisms promoting viral persistence can undermine cellular barriers to cancer.

Conclusions:

  • An evolutionary framework enhances understanding of why cancer mechanisms occur.
  • Infections, through evolutionary selection, can compromise cell cycle control, apoptosis, and cellular division limits, promoting oncogenesis.