imatinib

Overview

Small-molecule inhibitor of BCR-ABL, KIT, and PDGFRA.

Evidence in the corpus

  • Referenced in the Make-an-IMPACT rare-cancer program as a KIT-directed targeted therapy option relevant to histiocytosis and GCT cohorts profiled via MSK-IMPACT PMID:36862133.
  • Adjuvant imatinib context motivates a novel genomic risk stratification model for primary GIST: 41% of gastric and 53% of small bowel primary localized GISTs in the MSKCC cohort received adjuvant imatinib, and the authors propose genomic risk tiers to refine patient selection for adjuvant TKI therapy in the imatinib era PMID:37477937.
  • Invoked as the paradigmatic example of genotype-directed sarcoma therapy: recurrent activating KIT and PDGFRA mutations in GIST established the KIT → imatinib precedent that motivates subtype-specific targeted therapy across all soft-tissue sarcoma subtypes PMID:20601955.
  • SDH-deficient and NF1-related GISTs respond poorly to imatinib; in a cohort of 103 GIST patients with matched tumor-germline sequencing (MSK-IMPACT), 69% of KIT/PDGFRA-wildtype patients harbored germline P/LP variants (SDHA/SDHB/SDHC, NF1) rather than the KIT/PDGFRA targets imatinib acts on, highlighting that germline driver subtype guides TKI selection PMID:36593350
  • KIT mutations identified in melanoma tumors suggest potential sensitivity to imatinib in KIT-mutant cutaneous melanoma PMID:22622578
  • Activating KIT aberrations (V559A mutation, focal amplification) identified in BRAF/NRAS-WT melanoma subset (Broad, n=121); imatinib cited as a tyrosine kinase inhibitor with potential activity in KIT-aberrant melanoma PMID:22817889
  • One PDGFRA p.Thr674Ile-mutant sinonasal adenoid cystic carcinoma patient received imatinib as targeted therapy and was NED at 19 months — the only targeted-therapy case in an 88-case ACYC cohort PMID:24418857
  • Cited in the context of acquired resistance paradigms — analogous to ALK-fusion lung cancer/crizotinib and BRAF-mutant melanoma/vemurafenib — motivating combination regimens in HCC targeted therapy development PMID:24735922
  • Nominated for KIT-mutated/amplified Triple-WT melanoma subtype (14% of TCGA cases; no hot-spot BRAF/RAS/NF1); KIT mutations and 4q12 focal amplifications enriched in Triple-WT; imatinib/dasatinib proposed as targeted therapy based on prior Carvajal and Hodi reports PMID:26091043
  • KIT inhibitor; proposed as targeted therapy candidate for KIT-mutant GCT (mostly exon 17 hotspots, enriched in seminoma 29.6%); KIT exon 17 mutations in GCT represent an imatinib-resistance pattern distinct from GIST PMID:27646943
  • In 101 pediatric high-risk oncology patients (PIPseq), palliative imatinib produced near-complete clearing of peripheral blood blasts with a sustained 9-month response in a KIT Asn655Lys-mutant AML patient PMID:28007021

Resistance mechanisms

  • Not reported in corpus.

Cancer types (linked)

Sources

This page was processed by crosslinker on 2026-05-14. - PMID:22622578

This page was processed by crosslinker on 2026-05-14. - PMID:22817889

This page was processed by crosslinker on 2026-05-14. - PMID:24418857

This page was processed by crosslinker on 2026-05-14. - PMID:24735922

This page was processed by crosslinker on 2026-05-14. - PMID:26091043

This page was processed by crosslinker on 2026-05-14. - PMID:27646943

This page was processed by wiki-cli on 2026-05-14. - PMID:28007021 — Oberg et al. 2017, PIPseq; palliative imatinib in KIT Asn655Lys-mutant pediatric AML.

This page was processed by entity-page-writer on 2026-05-15.