Sunitinib, a multitargeted tyrosine kinase inhibitor, in the management of gastrointestinal stromal tumor

被引：19

作者：

George S. ^{[1
]}

机构：

[1] Center for Sarcoma and Bone Oncology, Dana-Farber Cancer Institute, Boston, MA 02115

来源：

Current Oncology Reports | 2007年 / 9卷 / 4期

关键词：

Gastrointestinal Stromal Tumor; Advanced Gist; Advanced Gastrointestinal Stromal Tumor; Clin Oncol Proc ASCO; Experimental Breast Cancer Bone Metastasis;

D O I：

10.1007/s11912-007-0040-1

中图分类号：

学科分类号：

摘要：

Due to the remarkable advances in the understanding of the biology of gastrointestinal stromal tumors (GIST), tyrosine kinase inhibition has become the mainstay of therapy for patients with advanced GIST. Sunitinib is a tyrosine kinase inhibitor with a wide range of kinase inhibition, including KIT, platelet-derived growth factor receptor (PDGFR), vascular endothelial growth factor (VEGF), and FLT3. Sunitinib has demonstrated benefit in patients with advanced GIST who have progressed on primary therapy with imatinib. The objectives of this review are to discuss the role of sunitinib in the current management of GIST, to review the unique side effect profile of the agent, and to discuss future trends in the use of the drug as the understanding of the mechanism of GIST evolves. Copyright © 2007 by Current Medicine Group LLC.

引用

页码：323 / 327

页数：4

共 37 条

[1]

Joensuu H., Fletcher C., Dimitrijevic S., Et al., Management of malignant gastrointestinal stromal tumors, Lancet Oncol, 3, pp. 655-664, (2002)

[2]

Emory T.S., Sobin L.H., Lukes L., Et al., Prognosis of gastrointestinal smooth muscle (stromal) tumors: Dependence on anatomic site, Am J Surg Pathol, 23, pp. 82-87, (1999)

[3]

Miettinen M., Monihan J.M., Sarlomo-Rikala M., Et al., Gastrointestinal stromal tumors/smooth muscle tumors (GISTs) primary in the omentum and mesentery: Clinicopathologic and immunohistochemical study of 26 cases, Am J Surg Pathol, 23, pp. 1109-1118, (1999)

[4]

Miettinen M., Sarlomo-Rikala M., Lasota J., Gastrointestinal stromal tumors: Recent advances in understanding of their biology, Hum Pathol, 30, pp. 1213-1220, (1999)

[5]

Nilsson B., Bumming P., Meis-Kindblom J.M., Et al., Gastrointestinal stromal tumors: The incidence, prevalence, clinical course, and prognostication in the preimatinib mesylate era - a population-based study in western Sweden, Cancer, 103, pp. 821-829, (2005)

[6]

Hirota S., Isozaki K., Moriyama Y., Et al., Gain-of-function mutations of c-kit in human gastrointestinal stromal tumors, Science, 279, pp. 577-580, (1998)

[7]

Heinrich M.C., Rubin B.P., Longley B.J., Fletcher J.A., Biology and genetic aspects of gastrointestinal stromal tumors: KIT activation and cytogenetic alterations, Hum Pathol, 33, pp. 484-495, (2002)

[8]

Heinrich M.C., Corless C.L., Duensing A., Et al., PDGFRA activating mutations in gastrointestinal stromal tumors, Science, 299, pp. 708-710, (2003)

[9]

Corless C.L., Schroeder A., Griffith D., Et al., PDGFRA mutations in gastrointestinal stromal tumors: Frequency, spectrum and in vitro sensitivity to imatinib, J Clin Oncol, 23, pp. 5357-5364, (2005)

[10]

National Comprehensive Cancer Network: Clinical Practice Guidelines in Oncology. Soft Tissue Sarcoma, GIST. v.1.2007, (2007)

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