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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

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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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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.
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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.
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Cancers arise due to mutations in genes involved in the regulation of cell division, which leads to unrestricted cell proliferation. Modern science and medicine have made great strides in the understanding and treatment of cancer, including eradicating cancer in some patients. However, there is still no cure for cancer. This is largely due to the fact that cancer is a large group of many diseases.
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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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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Updated: Jan 9, 2026

Characterizing Mutational Load and Clonal Composition of Human Blood
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Somatic mutations and clonal evolution in normal tissues and cancer development.

Kenichi Yoshida1

  • 1Division of Cancer Evolution, National Cancer Center Research Institute, Tokyo, Japan. keyoshi2@ncc.go.jp.

Experimental & Molecular Medicine
|December 2, 2025
PubMed
Summary
This summary is machine-generated.

Cancer initiation involves normal cells accumulating genetic mutations over decades, driven by aging and environment. Early driver mutations lead to clonal expansion, a key step in cancer development.

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Area of Science:

  • Genomic instability and cancer biology
  • Cellular and molecular oncology

Background:

  • Understanding early carcinogenesis is crucial for cancer prevention.
  • Analyzing genomic abnormalities in normal tissues was previously challenging.
  • Technological advances enable study of somatic mutation accumulation.

Purpose of the Study:

  • To review recent findings on somatic mutation accumulation in normal cells.
  • To discuss the acquisition of driver mutations.
  • To explore clonal evolution toward cancer.

Main Methods:

  • Review of recent scientific literature.
  • Analysis of genomic data from normal tissues.
  • Focus on somatic mutations, driver mutations, and clonal expansion.

Main Results:

  • Somatic mutations accumulate in normal cells due to aging and environmental factors.
  • Clonal expansion occurs when driver mutations are acquired.
  • Early driver mutations initiate a multi-decade process of clonal evolution.

Conclusions:

  • Cancer development is a gradual process starting with genetic alterations in normal cells.
  • Driver mutations play a critical role in clonal selection and expansion.
  • Further research into early carcinogenesis can inform cancer prevention strategies.