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Related Concept Videos

Replicative Cell Senescence02:15

Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...
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...
Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
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Loss of Tumor Suppressor Gene Functions

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Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

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.
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Such genes that act...
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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: Jul 11, 2026

Detecting Somatic Genetic Alterations in Tumor Specimens by Exon Capture and Massively Parallel Sequencing
11:02

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Published on: October 18, 2013

Somatic microsatellite mutations as molecular tumor clocks

D Shibata1, W Navidi, R Salovaara

  • 1Department of Pathology, University of Southern California School of Medicine, Los Angeles 90033, USA.

Nature Medicine
|June 1, 1996
PubMed
Summary

Microsatellite (MS) mutations reveal tumor evolution. Analyzing MS allele diversity in tumors provides direct estimates of cancer ages and reconstructs early tumor development, offering insights into mutator phenotype progression.

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Last Updated: Jul 11, 2026

Detecting Somatic Genetic Alterations in Tumor Specimens by Exon Capture and Massively Parallel Sequencing
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Area of Science:

  • Oncology
  • Genetics
  • Molecular Biology

Background:

  • Microsatellite (MS) mutations are key indicators in mutator phenotype tumors.
  • Tumor evolution is complex, with genetic diversity potentially correlating with tumor age.

Purpose of the Study:

  • To investigate the potential of microsatellite (MS) mutations to reconstruct the evolutionary history and age of mutator phenotype tumors.
  • To analyze MS allele diversity in various tumor types to understand early tumorigenesis.

Main Methods:

  • Characterization of MS allele diversity in xenografts, colorectal cancer with adjacent adenoma, and lung cancer metastasis.
  • Analysis of genetic diversity in relation to tumor duration and clinical presentation.

Main Results:

  • Rapid clonal expansions in xenografts showed homogenous MS alleles.
  • Colorectal cancer exhibited greater MS diversity compared to its adjacent adenoma.
  • Lung cancer metastasis displayed diversity consistent with its clinical duration and dormant phase.

Conclusions:

  • MS molecular tumor clocks can estimate tumor ages and reconstruct early tumor evolution.
  • Genetic diversity reflects the multistep process of tumorigenesis, including cell divisions and death rates.
  • MS analysis offers a unique tool for studying the occult evolution of human mutator phenotype tumors.