Related Experiment Video

Updated: Jun 21, 2026

Ultra-Fast Amplicon-Based Next-Generation Sequencing in Non-Squamous Non-Small Cell Lung Cancer
07:59

Ultra-Fast Amplicon-Based Next-Generation Sequencing in Non-Squamous Non-Small Cell Lung Cancer

Published on: September 8, 2023

Are RAS mutations predictive markers of resistance to standard chemotherapy?

Yohann Loriot1, Pierre Mordant, Eric Deutsch

  • 1SITEP, Department of Medicine, University Paris XI, Institut Gustave Roussy, Villejuif, France.

Nature Reviews. Clinical Oncology
|July 15, 2009
PubMed

Insights

KRAS mutations do not predict response to conventional chemotherapy in colorectal cancer (CRC) and non-small-cell lung cancer (NSCLC). These genetic markers should not guide decisions regarding traditional chemotherapy treatments.

Area of Science:

  • Oncology
  • Molecular Diagnostics
  • Cancer Therapeutics

Background:

  • KRAS mutations are known predictors of resistance to anti-EGFR therapies in colorectal cancer (CRC).
  • Their role in predicting response to conventional chemotherapy across various solid tumors remains less understood.
  • Current clinical practice may benefit from clarity on KRAS mutation utility beyond targeted therapy selection.

Purpose of the Study:

  • To comprehensively review the existing literature on the association between KRAS mutations and outcomes with conventional chemotherapy.
  • To determine if KRAS mutations serve as predictive biomarkers for conventional chemotherapy response in solid tumors.
  • To provide evidence-based recommendations on the clinical utility of KRAS mutation testing for chemotherapy selection.

Main Methods:

  • Systematic review of published studies investigating KRAS mutations and conventional chemotherapy response.
  • Inclusion of studies across multiple solid tumor types, including non-small-cell lung cancer (NSCLC) and CRC.
  • Analysis of data from both adjuvant and advanced treatment settings.

Main Results:

  • The review found no significant evidence supporting KRAS mutations as predictors of response to conventional chemotherapy.
  • This lack of predictive value was consistent across NSCLC, CRC, and other solid tumors.
  • Findings were observed in both adjuvant and advanced cancer treatment contexts.

Conclusions:

  • KRAS mutations are not valuable predictors of response to conventional chemotherapy in NSCLC, CRC, and other solid tumors.
  • Clinical decisions regarding conventional chemotherapy should not be based on KRAS mutation status.
  • Future research should focus on biomarkers that accurately predict response to conventional chemotherapy.

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...
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...
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...
Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
Three regulatory proteins control their activity:
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
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...