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Related Concept Videos

The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a superfamily...
Mutations01:39

Mutations

Overview
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...
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...
Abnormal Proliferation02:23

Abnormal Proliferation

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 daughter...
The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a superfamily...

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Related Experiment Video

Updated: May 14, 2026

Single Droplet Digital Polymerase Chain Reaction for Comprehensive and Simultaneous Detection of Mutations in Hotspot Regions
08:23

Single Droplet Digital Polymerase Chain Reaction for Comprehensive and Simultaneous Detection of Mutations in Hotspot Regions

Published on: September 25, 2018

KRAS mutation: should we test for it, and does it matter?

Patrick J Roberts1, Thomas E Stinchcombe

  • 1Lineberger Comprehensive Cancer Center, The University of North Carolina School of Medicine, Chapel Hill, NC 27599-7295, USA. patrick_roberts@unc.edu

Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology
|February 13, 2013
PubMed
Summary
This summary is machine-generated.

KRAS mutations are common in non-small-cell lung cancer (NSCLC) but don't predict chemotherapy benefit. EGFR mutation status is key for selecting patients for EGFR tyrosine kinase inhibitors.

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Fully Processed Recombinant KRAS4b: Isolating and Characterizing the Farnesylated and Methylated Protein
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Fully Processed Recombinant KRAS4b: Isolating and Characterizing the Farnesylated and Methylated Protein

Published on: January 16, 2020

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Lung cancer remains a leading cause of cancer mortality globally.
  • Non-small-cell lung cancer (NSCLC) classification has evolved to include molecular subsets.
  • KRAS mutations are the most frequent molecular alteration in NSCLC.

Purpose of the Study:

  • To review the biology of KRAS mutations in NSCLC.
  • To evaluate the predictive value of KRAS mutations for various therapies.
  • To discuss the integration of KRAS testing into clinical practice.

Main Methods:

  • Literature review of KRAS mutations in NSCLC.
  • Analysis of clinical utility for predicting treatment response.
  • Comparison with EGFR mutational status for targeted therapies.

Main Results:

  • KRAS mutations are associated with poor prognosis but lack predictive value for chemotherapy.
  • EGFR mutation status is the preferred biomarker for selecting patients for EGFR tyrosine kinase inhibitors.
  • No demonstrated association between KRAS status and benefit from anti-EGFR monoclonal antibodies.

Conclusions:

  • KRAS mutational analysis has limited clinical utility in NSCLC treatment selection.
  • EGFR testing is crucial for guiding EGFR tyrosine kinase inhibitor therapy.
  • Further research may clarify the role of KRAS in specific therapeutic contexts.