Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

KRAS and BRAF mutations predict primary resistance to imatinib in gastrointestinal stromal tumors.

Clinical cancer research : an official journal of the American Association for Cancer Research - 15 Mar 2012

Miranda Claudia, Nucifora Martina, Molinari Francesca, Conca Elena, Anania Maria Chiara, Bordoni Andrea, Saletti Piercarlo, Mazzucchelli Luca, Pilotti Silvana, Pierotti Marco A, Tamborini Elena, Greco Angela, Frattini Milo

Abstract excerpt

PURPOSE: Gastrointestinal stromal tumors (GIST) are characterized by gain-of-function mutations in KIT/PDGFRA genes leading to a constitutive receptor activation which is well counteracted by imatinib. However, cases in which imatinib as first-line treatment has no effects are reported (primary resistance). Our purpose is to investigate alterations in downstream effectors, not reported so far in mutated GIST,...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to 3T3 Cells
Share to Benzamides

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Gastrointestinal Neoplasms

Share to Gastrointestinal Stromal Tumors

Share to Imatinib Mesylate

Share to MAP Kinase Signaling System

Share to Piperazines

Share to Pyrimidines

Source

Identifiers

PMID: 22282465
DOI: 10.1158/1078-0432.CCR-11-2230

Genes

KIT
BRAF
KRAS
PDGFRA

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

KRAS and BRAF mutations predict primary resistance to imatinib in gastrointestinal stromal tumors.PMID 22282465Read ↗

Molecular mechanisms of secondary imatinib resistance in patients with gastrointestinal stromal tumors.Semantic proximity Read ↗

Mechanisms of secondary resistance to tyrosine kinase inhibitors in gastrointestinal stromal tumours (Review).Semantic proximity Read ↗

KIT and BRAF heterogeneous mutations in gastrointestinal stromal tumors after secondary imatinib resistance.Semantic proximity Read ↗

[Molecular mechanisms of primary and secondary resistance, molecular-genetic features and characteristics of KIT/PDGFRA non-mutated GISTs].Semantic proximity Read ↗

KIT/PDGFRA inhibitors for the treatment of gastrointestinal stromal tumors: getting to the gist of the problem.Semantic proximity Read ↗

Correlation of imatinib resistance with the mutational status of KIT and PDGFRA genes in gastrointestinal stromal tumors: a meta-analysis.Semantic proximity Read ↗

Resistance to Tyrosine Kinase Inhibitors in Gastrointestinal Stromal TumorsSemantic proximity Read ↗

Targeted therapy and personalized medicine in gastrointestinal stromal tumors: drug resistance, mechanisms, and treatment strategiesSemantic proximity Read ↗

Molecular basis for primary and secondary tyrosine kinase inhibitor resistance in gastrointestinal stromal tumor.Semantic proximity Read ↗

Clinical impact of primary and secondary KIT mutations on the efficacy of molecular-targeted therapies in gastrointestinal stromal tumors.Semantic proximity Read ↗

Mechanisms of resistance to imatinib mesylate in gastrointestinal stromal tumors and activity of the PKC412 inhibitor against imatinib-resistant mutants.Semantic proximity Read ↗

Novel Insights into the Treatment of Imatinib-Resistant Gastrointestinal Stromal Tumors.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.