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Related Concept Videos

Cancer02:18

Cancer

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.
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,...
Treatment Resistant Cancers02:56

Treatment Resistant Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
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,...

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Related Experiment Video

Updated: Jul 27, 2026

Identifying DNA Mutations in Purified Hematopoietic Stem/Progenitor Cells
11:06

Identifying DNA Mutations in Purified Hematopoietic Stem/Progenitor Cells

Published on: February 24, 2014

Cancer chemotherapy and somatic cell mutation.

M Kubota1, Y W Lin, K Hamahata

  • 1Department of Pediatrics, Faculty of Medicine, Kyoto University, Kawahara-cho 54, Shogoin, Sakyo-ku, 606-8507, Kyoto, Japan. Masaru.Kubota@ma2.seikyou.ne.jp

Mutation Research
|October 12, 2000
PubMed
Summary

Cancer chemotherapy can increase the risk of a second neoplasm. Understanding genotoxic effects and individual genetic factors is key to personalized cancer treatment and minimizing risks.

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Area of Science:

  • Oncology
  • Genetics
  • Pharmacology

Background:

  • Second neoplasms are a significant challenge in cancer chemotherapy.
  • Genotoxic effects of anti-cancer drugs are crucial for assessing cancer risk.
  • Somatic cell mutations and altered mutational spectra are observed post-chemotherapy.

Purpose of the Study:

  • To elucidate the genotoxic effects of anti-cancer drugs.
  • To identify factors influencing variability in chemotherapy-induced mutations.
  • To inform the development of individualized chemotherapy strategies.

Main Methods:

  • Somatic cell mutation assays.
  • Analysis of mutant frequency (Mf) at genetic loci (hprt, GPA, TCR).
  • Examination of mutational spectra of hprt mutants.

Main Results:

  • Chemotherapy increases in vivo somatic cell mutant frequency (Mf).
  • Mutations observed at hypoxanthine-guanine phosphoribosyl-transferase (hprt), glycophorin A (GPA), and T-cell receptor (TCR) loci.
  • Variability in mutation timing and degree suggests underlying genetic factors; elevated Mf seen in some pre-chemotherapy patients and those with cancer-prone syndromes.

Conclusions:

  • Individual genetic factors influence chemotherapy response and risk of secondary cancers.
  • Personalized chemotherapy approaches are necessary to minimize the risk of second neoplasms.
  • Somatic cell mutation assays provide valuable data for risk assessment and treatment individualization.