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Cancers Originate from Somatic Mutations in a Single Cell

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 Cell

Cancers Originate from Somatic Mutations in a Single Cell

Mutations

Mutations

Mutations

Mutations

Mutations are changes in the sequence of DNA. These changes can occur spontaneously or they can be induced by exposure to environmental factors. Mutations can be characterized in a number of different ways: whether and how they alter the amino acid sequence of the protein, whether they occur over a small or large area of DNA, and whether they occur in somatic cells or germline cells.
Chromosomal Alterations Are Large-Scale Mutations
While point mutations are changes in a single nucleotide in...

Mutations

Mutations

Mutations in Microorganisms

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,...

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Related Experiment Video

Updated: Mar 30, 2026

Characterizing Mutational Load and Clonal Composition of Human Blood

Characterizing Mutational Load and Clonal Composition of Human Blood

Published on: July 11, 2019

Clock-like mutational processes in human somatic cells.

Ludmil B Alexandrov^1,2,3, Philip H Jones^1,4, David C Wedge¹

¹Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, UK.

Nature Genetics

|November 10, 2015

Summary

This summary is machine-generated.

Scientists discovered two clock-like mutational signatures in human cells that accumulate mutations over time. These processes vary by tissue and may be influenced by cell division, offering insights into aging and cancer development.

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Last Updated: Mar 30, 2026

Characterizing Mutational Load and Clonal Composition of Human Blood

Characterizing Mutational Load and Clonal Composition of Human Blood

Published on: July 11, 2019

Studying Age-dependent Genomic Instability using the S. cerevisiae Chronological Lifespan Model

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Published on: September 29, 2011

Combining Magnetic Sorting of Mother Cells and Fluctuation Tests to Analyze Genome Instability During Mitotic Cell Aging in Saccharomyces cerevisiae

Combining Magnetic Sorting of Mother Cells and Fluctuation Tests to Analyze Genome Instability During Mitotic Cell Aging in Saccharomyces cerevisiae

Published on: October 16, 2014

Area of Science:

Genomics
Cancer Biology
Molecular Epidemiology

Background:

Somatic cells accumulate mutations throughout life due to various mutational processes.
Each process leaves a distinct mutational signature on the genome.
Some age-related mutational processes occur at a constant rate, proportional to chronological age.

Purpose of the Study:

To investigate clock-like mutational processes in normal human somatic cells.
To identify and characterize mutational signatures that exhibit age-dependent accumulation.
To explore the biological influences and tissue-specific variations of these processes.

Main Methods:

Analysis of mutations from 10,250 cancer genomes across 36 cancer types.
Identification of mutational signatures with clock-like properties.
Comparison of mutation rates across different human tissues.

Main Results:

Two distinct mutational signatures exhibiting clock-like properties were identified.
Both signatures showed tissue-specific mutation rates.
The mutation rates of the two signatures were not correlated, suggesting different underlying biological drivers.
One signature's rate may be influenced by the rate of cell division.

Conclusions:

This study presents the first comprehensive survey of clock-like mutational processes in human somatic cells.
Identified signatures provide insights into the aging process and potentially cancer development.
The findings highlight the complexity of mutational processes and their tissue-specific regulation.