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Related Experiment Video

Updated: Jul 3, 2026

Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure

Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure

Published on: August 11, 2017

KRAS mutations predict response to EGFR inhibitors.

Mitch Raponi¹, Hans Winkler, Nicholas C Dracopoli

¹Centocor R&D, 145 King of Prussia Road, Radnor, PA 19086, USA. mraponi1@cntus.jnj.com

Current Opinion in Pharmacology

|July 16, 2008

Summary

KRAS mutations can predict patient response to anti-epidermal growth factor receptor (EGFR) therapies. Identifying KRAS status helps exclude patients unlikely to benefit from these cancer treatments.

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Deciphering the Structural Effects of Activating EGFR Somatic Mutations with Molecular Dynamics Simulation

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Last Updated: Jul 3, 2026

Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure

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Published on: August 11, 2017

Deciphering the Structural Effects of Activating EGFR Somatic Mutations with Molecular Dynamics Simulation

Deciphering the Structural Effects of Activating EGFR Somatic Mutations with Molecular Dynamics Simulation

Published on: May 20, 2020

Area of Science:

Oncology
Molecular Biology
Genetics

Background:

Anti-epidermal growth factor receptor (EGFR) therapies are approved for solid tumors.
Current response rates for anti-EGFR therapy are low.
Biomarkers can identify patients likely to respond to anti-EGFR therapy.

Purpose of the Study:

To evaluate the utility of KRAS mutational status as a predictive biomarker for anti-EGFR therapy.
To determine if KRAS mutations can identify patients unlikely to benefit from anti-EGFR therapy.

Main Methods:

Review of clinical data on anti-EGFR therapies.
Analysis of KRAS gene mutations in tumor samples.
Correlation of KRAS mutational status with patient response to anti-EGFR therapy.

Main Results:

KRAS acts downstream of the EGFR in signal transduction pathways.
Somatic mutations in KRAS can be used to exclude patients unlikely to benefit from anti-EGFR therapy.
Clinical data support KRAS mutational status as a diagnostic marker for predicting response.

Conclusions:

KRAS mutational status is a valuable diagnostic marker for predicting response to anti-EGFR therapies.
Utilizing KRAS status can improve patient selection for anti-EGFR therapy in colorectal and non-small cell lung cancer.
KRAS testing can help personalize cancer treatment strategies.