Oncology
Gastrointestinal Stromal Tumor
Also known as GIST, KIT/PDGFRA tumor, gastrointestinal stromal sarcoma
Gastrointestinal stromal tumours are the most common mesenchymal tumours of the GI tract, arising from the interstitial cells of Cajal or their precursors, and defined by gain-of-function mutations in KIT (approximately 80%) or PDGFRA (appr
58
studies recruiting now
as of 7 Sept 2026
431
studies registered in total
as of 7 Sept 2026
23
countries with a recruiting site
as of 7 Sept 2026
15 Aug 2025
most recent study posted
among recruiting studies
Recruiting trials
A Study to Learn More About How Well Treatment With Sevabertinib (BAY 2927088) Tablets Works and How Safe it is in Participants Who Have a Solid Tumor With Mutations of the Human Epidermal Growth Factor Receptor 2 (HER2)
Belzutifan/MK-6482 for the Treatment of Advanced Pheochromocytoma/Paraganglioma (PPGL), Pancreatic Neuroendocrine Tumor (pNET), Von Hippel-Lindau (VHL) Disease-Associated Tumors, Advanced Gastrointestinal Stromal Tumor (wt GIST), or Solid Tumors With HIF-2α Related Genetic Alterations (MK-6482-015)
Imatinib TDM in GIST
DESTINY-PANTUMOUR04
Showing the 5 most recently updated recruiting studies, as recorded 7 Sept 2026. Live status on each study page.
See all 58 recruiting studiesWhere recruiting studies are running
Countries with at least one recruiting site among the studies above, 7 Sept 2026. Tap a country to search trials there.
Keep watching
Get an email when a new Gastrointestinal Stromal Tumor study opens.
One email a day at most. Unsubscribe with one click.
Used only for these alerts. Privacy.
Support
Patient organisations
Registry: Life Raft Group Patient Registry · Join ↗. Registries connect patients to researchers and often hear about trials first.
About Gastrointestinal Stromal Tumor
Gastrointestinal stromal tumours are the most common mesenchymal tumours of the GI tract, arising from the interstitial cells of Cajal or their precursors, and defined by gain-of-function mutations in KIT (approximately 80%) or PDGFRA (approximately 10%), with the remaining cases being wild-type and often harbouring SDH complex deficiency, NF1 mutations, or BRAF alterations. The advent of imatinib and subsequent generations of tyrosine kinase inhibitors has transformed the management of advanced GIST, but drug resistance through secondary KIT/PDGFRA mutations remains the central clinical challenge. Precise molecular subtyping of the primary driver mutation is essential for predicting drug sensitivity and determining eligibility for targeted therapy trials.
Common clinical features
From Orphanet’s phenotype annotations (CC BY 4.0). Not a complete list.
Treatments being studied
6 approved treatments and 51 in clinical development, from Open Targets (CC BY 4.0). Not medical advice.
+ 43 more in development
Before you apply
Things trial teams commonly ask about for Gastrointestinal Stromal Tumor. Not eligibility rules; those are set by each study.
- Precise molecular characterisation — KIT exon 9, 11, 13, or 17 mutation, PDGFRA mutation including D842V status, or SDH/NF1/BRAF wild-type subtype — is required for virtually all targeted therapy trials and determines which TKI is applicable.
- PDGFRA D842V mutations confer resistance to imatinib and sunitinib but sensitivity to avapritinib; confirm D842V status separately as standard KIT/PDGFRA panels do not always report this variant explicitly.
- Prior TKI lines of therapy and reasons for discontinuation (progression vs. toxicity) are key eligibility variables; provide a complete treatment chronology with best response and progression dates for each agent.
Related conditions
Information, not medical advice. Trial listings are shown as recorded on ClinicalTrials.gov; whether any study is right for you is a decision for you and your clinicians, and eligibility is decided by each research team. Disease information from Orphanet (CC BY 4.0).