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1 ective in first-line treatment of metastatic gastrointestinal stromal tumour.
2 lacebo after resection of localised, primary gastrointestinal stromal tumour.
3 with placebo after the resection of primary gastrointestinal stromal tumour.
4 y be performed in all patients with advanced gastrointestinal stromal tumour.
5 he study included patients with unresectable gastrointestinal stromal tumours.
6 n patients with previously treated, advanced gastrointestinal stromal tumours.
7 d with sunitinib in patients with metastatic gastrointestinal stromal tumours.
8 transformation of ICC and the development of gastrointestinal stromal tumours.
9 linical challenge for patients with advanced gastrointestinal stromal tumours.
10 n patients with advanced PDGFRA D842V-mutant gastrointestinal stromal tumours.
11 pared with placebo in patients with advanced gastrointestinal stromal tumour after failure and discon
12 in the treatment of recurrent or metastatic gastrointestinal stromal tumours and is now being tested
13 uding 20 patients with a PDGFRA D842V-mutant gastrointestinal stromal tumour, and 36 patients with a
16 ts had complete gross resection of a primary gastrointestinal stromal tumour at least 3 cm in size an
17 nts with metastatic renal-cell carcinoma and gastrointestinal stromal tumours, but concerns have aris
18 nal involvement in adenocarcinoma, lymphoma, gastrointestinal stromal tumours, Crohn's disease, and g
20 opulation (patients with PDGFRA D842V-mutant gastrointestinal stromal tumour from the dose-escalation
21 approved as third-line therapy for advanced Gastrointestinal Stromal Tumour (GIST) at a starting dos
25 ave proven clinical benefit in patients with gastrointestinal stromal tumours (GIST), but almost all
29 initiating events, fostering hyperplasia in gastrointestinal stromal tumours (GISTs), and additional
31 vant imatinib therapy for many patients with gastrointestinal stromal tumours (GISTs); however, its o
32 RA with imatinib revolutionised treatment in gastrointestinal stromal tumour; however, PDGFRA Asp842V
33 rt and all patients with PDGFRA D842V-mutant gastrointestinal stromal tumour in the dose-expansion pa
34 bits PDGFRA D842V, in patients with advanced gastrointestinal stromal tumours, including patients wit
35 r; however, PDGFRA Asp842Val (D842V)-mutated gastrointestinal stromal tumour is highly resistant to t
39 on of isolated metastatic colorectal cancer, gastrointestinal stromal tumours, neuroendocrine cancers
40 apparent antitumour activity was noted in a gastrointestinal stromal tumour, papillary thyroid cance
42 nts with an unresectable PDGFRA D842V-mutant gastrointestinal stromal tumour regardless of previous t
43 anced breast cancer and rare tumours such as gastrointestinal stromal tumours, sarcoma, thyroid cance
44 y data, and evolving knowledge regarding the gastrointestinal stromal tumour treatment paradigm, it w
45 , and 36 patients with a PDGFRA D842V-mutant gastrointestinal stromal tumour were enrolled in the dos
46 e intracellular Bcr-Abl tyrosine kinase, and gastrointestinal stromal tumours, where it targets eithe
47 sed in all patients with PDGFRA D842V-mutant gastrointestinal stromal tumour who received avapritinib
48 kinase inhibitor, in patients with advanced gastrointestinal stromal tumour who were resistant to or
49 atients with imatinib-resistant, metastatic, gastrointestinal stromal tumours who had been enrolled i
50 ble safety profile in patients with advanced gastrointestinal stromal tumours who were resistant to a
51 mal tumour regardless of previous therapy or gastrointestinal stromal tumour with other mutations tha
52 ents aged 18 years or older who had advanced gastrointestinal stromal tumours with progression on at
53 chromocytoma/paraganglioma (PPGL), wild type gastrointestinal stromal tumour (wtGIST) and renal cell