KIT mutation

P1/2, N=94, Recruiting, Deciphera Pharmaceuticals, LLC | Not yet recruiting --> Recruiting

P2, N=48, Recruiting, Asan Medical Center | Trial completion date: Dec 2026 --> Dec 2027 | Trial primary completion date: Aug 2026 --> Aug 2027

P2, N=28, Recruiting, Asan Medical Center | Not yet recruiting --> Recruiting

Since the introduction of imatinib in the early 21st century, the management of metastatic GIST has shifted from solely surgical intervention to a systemic, chronic disease management model centered on tyrosine kinase inhibitors (TKIs)...These challenges underscore the necessity of this review, which discusses current standard drug treatment strategies for advanced GIST, including sequential TKIs therapy and investigations into mechanisms of drug resistance. Finally, the review explores precise and actionable future directions for GIST drug development and clinical management, including mutation-stratified therapeutic sequencing, rational TKI-based combination regimens, and circulating tumor DNA (ctDNA)-guided real-time treatment monitoring and resistance surveillance.

P2, N=40, Completed, Asan Medical Center | Recruiting --> Completed

P1/2, N=48, Recruiting, Asan Medical Center | Not yet recruiting --> Recruiting

The median overall survival was 35.1 months for AML with RUNX1::RUNX1T1 versus 24.0 months for other AML (p = 0.0797) and 28.1 months in patients with KIT mutations versus 25.6 months in those without (p = 0.9051). These data highlight a strong biological association between RUNX1::RUNX1T1 and KIT exon 17 mutations and underscore the need for prospectively designed studies and the evaluation of KIT-directed therapeutic strategies in this subset of patients with AML.

P1, N=18, Recruiting, University of California, San Diego | Not yet recruiting --> Recruiting | Initiation date: Dec 2025 --> Jun 2026

CK and KIT mutations jointly identify a high-risk subgroup within t(8;21) AML. This baseline genetic stratification provides a foundation for risk-adapted therapy, with MRD assessment at CR offering complementary prognostic information.

c-KIT mutations resulted in 35% of the children tested. The RT-PCR technique resulted more sensitive in finding c-KIT D816V, while NGS in detecting other mutations whose prognostic roles require further investigation.

The validity of the Idylla IDH1-2 Mutation Assay was 98.06%. The Idylla IDH1-2 Mutation Assay Kit showed comparable performance to other well-validated methods for IDH mutation analysis while demonstrating excellent assay turnaround times.

Here, we summarize current knowledge of KIT expression and the functional consequences of Kit mutations, with particular emphasis on oocytes across ovarian cell populations and in comparison to other organ systems in humans and mice. We further evaluate the physiological and pathological significance of ovarian KIT signaling in female fertility and highlight crucial knowledge gaps that must be addressed to fully elucidate its role in maintaining ovarian function.