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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
PubMed

Insights

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.

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.

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