View clinical trials related to Gastrointestinal Stromal Tumors.
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This phase II trial studies how well linsitinib works in treating younger and adult patients with gastrointestinal stromal tumors. Linsitinib may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth.
KIT exon 9 mutants had poorer survival compared with KIT exon 11 mutants when they were treated with the same dose of imatinib, 400 mg per day, and that patients with KIT exon 9 mutation had better progression-free survival with imatinib treatment at an escalated dose, 800 mg per day, than with imatinib treatment at a dose of 400 mg per day.10,11 Based on the results, imatinib 800 mg per day is now considered the standard dose for the treatment of patients with metastatic or unresectable GIST showing KIT exon 9 mutation in Western countries.
Patients with metastatic or locally advanced gastrointestinal stromal tumors (GIST) who develop resistance against the two hitherto approved drugs for this disease, the tyrosin kinase inhibitors (TKIs) imatinib and sunitinib, have a poor prognosis. Sometimes a further response may be achieved by other drugs, mainly other TKIs, which have been explored in different studies but not yet have been approved for clinical use. Pazopanib is a TKI inhibiting the tyrosin kinases KIT, PDGFRA, and VEGF 1-3, all of which have important roles in the pathogenesis of GIST. Theoretically, it may function in GIST, and it deserves investigational trials. The drug is approved for metastatic renal cancer and is relatively well tolerated. In this trial (SSG XXI), the disease control rate (DCR) = (CR+PR+SD) after 12 weeks of treatment will be assessed as the primary endpoint, and at the same time trough levels will be measured. Secondary endpoints include ORR, PFS, toxicity, and disease control rate in relation to trough level week 12 and in relation to the primary mutation of the tumor (if known). The goal is to include 72 patients in the trial, which is open and single arm.
The objective is to compare efficacy and safety of masitinib at 12 mg/kg/day to sunitinib at 50 mg/day in treatment of patients with gastro-intestinal stromal tumor resistant to imatinib.
Mutations of tumor-related genes are dynamic. Gastrointestinal stromal tumor cells often are obviously more invasive in case of recurrence. The great majority of relapses may be associated with secondary mutation in the GIST related genes. Full gene sequences of c-KIT、PDGFRA and DOG1, which is extracted from the specimen cells of repeated surgical resection or biopsy tissue in GIST patients with postoperative recurrence, are analyzed with the screening-sequencing approach, in order to investigate the characteristics and variations associated with the different gene mutations of c-KIT、PDGFRA and DOG1 in GIST patients and be likely to find out the evolutionary pattern, try to learn the facts about the effect of tyrosine kinase inhibitors on the GIST related genes, make a survey of any association of c-KIT、PDGFRA and DOG1 gene mutations and provide the basis for seeking molecular marker of GIST for monitoring course of disease, and offer a theoretical basis and new therapeutic strategies for application of clinical treatment.
This study will evaluate the efficacy, safety, tolerability of imatinib in the neoadjuvant treatment (pre-operatory) of patients with GIST. It will also evaluate the potential of imatinib to convert a tumor from inoperable to operable.
The purpose of this study is to evaluate the efficacy and safety of Dovitinib in patients with gastrointestinal stromal tumors refractory and/or intolerant to Imatinib
The purpose of this study is to determine a maximum tolerated dose and/or recommended phase 2 dose of a combination of imatinib and BKM120 in the treatment of 3rd line GIST patients.
Activating mutations of the kinases CKIT or PDGFRA can be detected in 90% of cases by DNA sequence analysis of a pathological specimen. These mutated genomic DNA fragments are highly specific for the tumor and are released by the tumor into the circulation. Allele-specific PCR can be used to specifically amplify and quantify mutated CKIT and PDGFR DNA fragments. The current trial aims to evaluate whether tumor DNA carrying mutations for CKIT and PDGFRA can be detected and quantified in the plasma of patients with active GIST, and whether detection can be correlated with the clinical course of disease either under therapy or in progressive disease irrespective of current therapy.