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Related Concept Videos

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...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

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,...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

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,...
What is Cancer?02:12

What is Cancer?

Cells and tissues must meticulously coordinate their activities for the normal functioning of the human body. Therefore, they exhibit socially responsible behavior - resting, growing, dividing, differentiating, or dying - for the organism’s benefit. Cancer arises when cells divide uncontrollably and invade other tissues or organs.
Although people have known about cancer for centuries, it was only in 1761 that Giovanni Morgagni of Padua performed a detailed autopsy of patients who died from...
Mouse Models of Cancer Study02:43

Mouse Models of Cancer Study

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,...

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Related Experiment Video

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The Drosophila Imaginal Disc Tumor Model: Visualization and Quantification of Gene Expression and Tumor Invasiveness Using Genetic Mosaics
10:31

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Published on: October 6, 2016

Cancer models, genomic instability and somatic cellular Darwinian evolution.

Mark P Little1

  • 1Department of Epidemiology and Biostatistics, School of Public Health, Imperial College Faculty of Medicine, London, UK. mark.little@imperial.ac.uk

Biology Direct
|April 22, 2010
PubMed
Summary

Cancer development is modeled as a somatic cellular evolutionary process, supported by genomic instability (GI). This review examines evolutionary carcinogenesis models, including multi-stage and mutation-based hypotheses.

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Area of Science:

  • Evolutionary Biology
  • Cancer Research
  • Genetics

Background:

  • Cancer biology is complex, involving cellular and genetic alterations.
  • Genomic instability (GI) is implicated in cancer development.
  • Existing models attempt to explain carcinogenesis mechanistically.

Purpose of the Study:

  • To critically review the evolutionary biology of cancer.
  • To examine the role of genomic instability in carcinogenesis.
  • To analyze quasi-mechanistic models of cancer development based on evolutionary principles.

Main Methods:

  • Literature review of cancer biology and evolutionary theory.
  • Analysis of evidence for cancer as a somatic cellular Darwinian evolutionary process.
  • Review of established carcinogenesis models (e.g., Armitage-Doll, Moolgavkar-Venzon-Knudson) and their generalizations incorporating GI.

Main Results:

  • Evidence supports modeling cancer development as a somatic cellular evolutionary process.
  • Genomic instability plays a significant role in carcinogenesis.
  • Various evolutionary models, including multi-stage and mutation-based approaches, provide frameworks for understanding cancer progression.

Conclusions:

  • Cancer's development can be effectively modeled as a Darwinian evolutionary process at the somatic cellular level.
  • Genomic instability is a key factor contributing to this evolutionary process.
  • Existing mathematical models offer valuable insights into the multi-stage nature of carcinogenesis.