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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...
Mutagenicity and Carcinogenicity01:25

Mutagenicity and Carcinogenicity

Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...
Mismatch Repair01:20

Mismatch Repair

Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
Mismatch Repair01:36

Mismatch Repair

Overview
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...

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Related Experiment Video

Updated: May 13, 2026

Comparative Lesions Analysis Through a Targeted Sequencing Approach
08:16

Comparative Lesions Analysis Through a Targeted Sequencing Approach

Published on: November 5, 2019

Somatic mutation patterns and compound response in cancers.

Ningning He1, Nayoung Kim, Sukjoon Yoon

  • 1Department of Biological Sciences, Sookmyung Women's University, Seoul 140-742, Korea.

BMB Reports
|February 26, 2013
PubMed
Summary
This summary is machine-generated.

Researchers screened ~40,000 compounds against cancer cell lines with specific mutations. Over 1,000 compounds showed mutation-specific drug responses, revealing new therapeutic strategies for anti-cancer agents.

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Implementation of In Vitro Drug Resistance Assays: Maximizing the Potential for Uncovering Clinically Relevant Resistance Mechanisms
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Detecting Somatic Genetic Alterations in Tumor Specimens by Exon Capture and Massively Parallel Sequencing
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Detecting Somatic Genetic Alterations in Tumor Specimens by Exon Capture and Massively Parallel Sequencing

Published on: October 18, 2013

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Last Updated: May 13, 2026

Comparative Lesions Analysis Through a Targeted Sequencing Approach
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Published on: November 5, 2019

Implementation of In Vitro Drug Resistance Assays: Maximizing the Potential for Uncovering Clinically Relevant Resistance Mechanisms
08:46

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

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

Published on: October 18, 2013

Area of Science:

  • Oncology
  • Pharmacology
  • Genomics

Background:

  • Cancer cell lines with defined mutations model tumor-associated genetic alterations.
  • Understanding mutation-drug response relationships is crucial for targeted cancer therapy.

Purpose of the Study:

  • To analyze the effects of a large compound library on diverse cancer cell lines.
  • To identify compounds with mutation-dependent sensitivity profiles.
  • To discover novel relationships between somatic mutations and chemical compound responses.

Main Methods:

  • Utilized ~40,000 compounds for screening against various cancer cell lines.
  • Characterized mutation-dependent sensitivity profiles across cell lines.
  • Clustered compounds based on mutation-oriented sensitivity patterns.

Main Results:

  • Identified over 1,000 compounds with unique sensitivity to specific cancer cell line genotypes.
  • Discovered six distinct classes of mutation-oriented drug sensitivity.
  • Established a link between somatic mutations and the selective response of chemical compounds.

Conclusions:

  • The study provides significant insights into genotype-specific drug responses in cancer.
  • Findings can aid in predicting and optimizing therapeutic windows for anti-cancer drugs.
  • This research supports the development of personalized anti-cancer therapies based on mutation profiles.