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Association details:
| Biomarker: | KIT exon 11 mutation |
|---|---|
| Cancer: | Gastrointestinal Stromal Tumor |
| Drug: | imatinib (c-KIT inhibitor, Bcr-abl tyrosine kinase inhibitor, PDGFR inhibitor) |
| Direction: | Sensitive |
Evidence:
Source:
Title:
Prospective Multicenter Clinical Study of Neoadjuvant Imatinib Mesylate for Gastrointestinal Stromal Tumors
Excerpt:
...- Gene mutation test report including c-kit exons 9,11,13 and 17 and platelet-derived growth factor receptor alpha (PDGFRA) exons 12 and 18...
Trial ID:
Source:
Title:
Adjuvant Imatinib in High-risk Gastrointestinal Stromal Tumor (GIST) With C-kit Mutation
Excerpt:
...- Presence of mutation in exon 11 of c-kit gene....
Trial ID:
Less C2 evidence
Source:
Title:
1513P - Impact of mutational status on long-term treatment outcomes in patients with advanced gastrointestinal stromal tumors (GIST) treated in the first line with imatinib
Published date:
09/05/2022
Excerpt:
Prospectively collected data of patients with advanced GIST with known mutational status (KIT/PDGFRA) and treated with imatinib between 01/2001 and 12/2021 were analyzed…. In multivariate analysis factors correlated with longer PFS in gastric GIST were: female gender (HR 0.60; 95%CI 0.37-0.97) and KIT ex 11 point mutations (HR 0.22; 0.70-0.73), while in non-gastric GIST: KIT ex 11 codon 557-558 deletions (HR 0.43; 0.24-0.75), point mutations (HR 0.48; 0.27-0.87) or other KIT ex 11 alterations (HR 0.40; 0.23-0.70) and no PDGFRA ex 18 D842V mutation (HR 0.11; 0.04-0.34). Only factors associated with OS in gastric GIST were: female gender (HR 0.41; 95%CI 0.24-0.70) and no PDGFRA ex 18 D842V mutation (HR 0.32; 0.14-0.71), while KIT ex 11 other deletions/indels/duplications (HR 0.57; 0.36-0.88) in non-gastric GIST.
Title:
Clinicopathological characteristics and prognostic analysis of KIT/PDGFRA gene "homozygous" mutations in gastrointestinal stromal tumors: a multicenter retrospective cohort study
Published date:
09/25/2021
Excerpt:
In 60 cases of recurrent or metastatic GISTs with KIT gene exon 11 mutation, IM was used as the first-line treatment, and the progression-free survival (PFS) of GISTs with "homozygous mutation" was shorter compared to GISTs with "heterozygous mutation" (median PFS: 38 months vs. 69 months, P=0.044). The differences were statistically significant.
DOI:
10.3760/cma.j.cn.441530-20210720-00293
Source:
Title:
The analysis of 3-year adjuvant therapy with imatinib in patients with high-risk molecular profiled gastrointestinal stromal tumors (GIST) treated in routine practice
Published date:
08/16/2020
Excerpt:
CONFLICTING EVIDENCE: The majority of GIST cases harboured exon 11 KIT mutations (88 cases, 82%), 11 cases had exon 9 KIT mutations (10%), 8 had other KIT/PDGFRA mutations potentially sensitive to imatinib. The disease relapse was detected in 19 patients, of them in 5 cases in exon 9 KIT mutants (45%), and 14 cases in patients with exon 11 KIT mutations (11%) [p < 0.01].
DOI:
10.1016/j.ejso.2020.08.004
Source:
Title:
Clinicopathological and Molecular Characterization of Metastatic Gastrointestinal Stromal Tumors with Prolonged Benefit to Frontline Imatinib
Published date:
08/20/2019
Excerpt:
Sixty-four imatinib long-term responders (LTRs) and 70 control cases were identified. Compared with controls...KIT exon 11 was the only region found mutated in LTRs.
DOI:
10.1634/theoncologist.2018-0032
