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Activation of ERBB2 signaling causes resistance to the EGFR-directed therapeutic antibody cetuximab.

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Sci Transl Med2011PMID 21900593PMC3268675stubpubmedProvenance
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 (4)

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Validated 4

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
21900593
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
NRG1 Expression1
CetuximabMalignant Colorectal NeoplasmCURATED_BROADERPredictiveDSupports Resistance4accepted
EID777

NRG1 upregulation or ERBB2 amplification were the main causes of resistance to cetuximab in-vivo and in-vitro in this study. Inhibition of ERBB2/ERBB3 signaling restored cetuximab sensitivity.

PMID 21900593 · Yonesaka et al., 2011 · Open in CIViC

civic