Phase II trial of nilotinib as third-line therapy for gastrointestinal stromal tumor (GIST) patients in Japan.

Nishida, Tomoki; Sawaki, Akira; Doi, T.; Yamada, Yukinori; Kanda, Tatsuo; Kakeji, Yoshihiro; Onozawa, Yusuke; Yamasaki, M.; Ohtsu, A.

doi:10.1200/jco.2010.28.15_suppl.10015

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Medical Management Of Gastrointestinal Stromal Tumor With Im1

New Tki's That Inhibit Kit and Pdgfr1

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Cited by 7 publications

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“…There are multiple TKIs under development and in various stages of investigation including nilotinib [92][93][94], sorafenib [95][96][97], masitinib [98,99], regorafenib [100], dasatinib [101,102], and vatalanib [103]. Crenolanib is a novel PDGFR kinase inhibitor undergoing evaluation in GIST patients whose tumors carry a PDGFRA D842V mutation to most other kinases available [104].…”

Section: Medical Management Of Gastrointestinal Stromal Tumor With Immentioning

confidence: 99%

Small intestine gastrointestinal stromal tumors

Grover¹,

Ashley²,

Raut³

2012

Current Opinion in Gastroenterology

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Section: Medical Management Of Gastrointestinal Stromal Tumor With Immentioning

confidence: 99%

Small intestine gastrointestinal stromal tumors

Grover¹,

Ashley²,

Raut³

2012

Current Opinion in Gastroenterology

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“…Median progression‐free survival was 3 months with a median overall survival of 8.5 months. A phase II trial further confirmed activity of nilotinib in the third‐line setting with 35 patients enrolled and 24 patients (69%) demonstrating benefit (1PR and 23 SD) with a median progression‐free survival of 4 months and median overall survival of 11 months 16. A phase III trial was conducted in 248 patients who had failed both imatinib and sunitinib randomized 2:1 to either nilotinib or best supportive care 17.…”

Section: New Tki's That Inhibit Kit and Pdgfrmentioning

confidence: 92%

Systemic therapy for advanced gastrointestinal stromal tumors: Beyond imatinib

Kim

Zalupski

2011

Journal of Surgical Oncology

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Progression on first-line therapy with imatinib in gastrointestinal stromal tumors (GIST) is caused by either initial resistance or more often a secondary mutation in tyrosine kinases KIT or PDGFR. Therapies in development for imatinib-resistant GIST include agents that target KIT/PDGFR with greater potency or possess broader kinase inhibition profiles including VEGFR. To circumvent secondary mutations in KIT/PDGFR, inhibition of the downstream signaling in PI3K/Akt/mTOR pathway and enhanced degradation of KIT/PDGFR are also under investigation.

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