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KRAS mutations and primary resistance of lung adenocarcinomas to gefitinib or erlotinib.

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PLoS Med2005PMID 15696205PMC545207stubpubmedProvenance
Source
PubMed
Retrieved
Sep 8, 2026
Layer
normalized (units and labels harmonized; values unchanged)
Run
ING-CIVIC-20260908-000001
Published

Abstract

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Linked entities

Linked entities (5)

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Validated 5

Curated evidence

Evidence citing this paper (1)

civicProvenance
Source
CIViC — Clinical Interpretation of Variants in Cancer
Dataset
CIViC evidence items
Version
civic-2026-09-08
Retrieved
Sep 8, 2026
Layer
normalized (units and labels harmonized; values unchanged)
Evidence
expert curation
License
CC0 1.0
PMID
15696205
Run
ING-CIVIC-20260908-000001
Open at source
CuratedShowing 1–1 of 1 evidence items · levels, directions and significance as curated at the source; each row links to its CIViC record.
TherapyCancerTypeLevelDirection · significanceRating (1–5)StatusEvidenceSource
KRAS G12/G131
Erlotinib + GefitinibSubstitutesLung Non-Small Cell CarcinomaCURATED_BROADERPredictiveBSupports Resistance3accepted
EID35

In 60 patients with NSCLC, Exon 2 KRAS mutations were associated with resistance to the EGFR kinase inhibitors gefitinib or erlotinib (9/38 refractory vs 0/21 sensitive patients; P=0.0201).

PMID 15696205 · Pao et al., 2005 · Open in CIViC

civic