RESEARCH
Year : 2005  |  Volume : 4  |  Issue : 1  |  Page : 19

The role of c-kit and imatinib mesylate in uveal melanoma


1 Department of Ophthalmology, Federal University of São Paulo, São Paulo, Brazil; Henry C. Witelson Ocular Pathology Laboratory, Department of Ophthalmology, McGill University, Montreal – Canada
2 Henry C. Witelson Ocular Pathology Laboratory, Department of Ophthalmology, McGill University, Montreal – Canada
3 Department of Ophthalmology, Federal University of São Paulo, São Paulo, Brazil

Correspondence Address:
Alexandre Nakao Odashiro
Department of Ophthalmology, Federal University of São Paulo, São Paulo, Brazil; Henry C. Witelson Ocular Pathology Laboratory, Department of Ophthalmology, McGill University, Montreal – Canada

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Source of Support: None, Conflict of Interest: None


DOI: 10.1186/1477-3163-4-19

Background: Uveal melanoma (UM) is the most common primary intraocular tumor in adults, leading to metastasis in 40% of the cases and ultimately to death in 10 years, despite local and/or systemic treatment. The c-kit protein (CD117) is a membrane-bound tyrosine kinase receptor and its overexpression has been observed in several neoplasms. Imatinib mesylate is a FDA approved compound that inhibits tyrosine quinase receptors, as well as c-kit. Imatinib mesylate controls tumor growth in up to 85% of advanced gastrointestinal stromal tumors, a neoplasia resistant to conventional therapy. Methods: Fifty-five specimens of primary UM selected from the archives of the Ocular Pathology Laboratory, McGill University, Montreal, Canada, were immunostained for c-kit. All cells displaying distinct immunoreactivity were considered positive. Four human UM cell lines and 1 human uveal transformed melanocyte cell line were tested for i n vitro proliferation Assays (TOX-6) and invasion assay with imatinib mesylate (concentration of 10 μM). Results: The c-kit expression was positive in 78.2% of the UM. There was a statistical significant decrease in the proliferation and invasion rates of all 5 cell lines. Conclusion: The majority of UM expressed c-kit, and imatinib mesylate does decrease the proliferation and invasion rates of human UM cell lines. These results justify the need for a clinical trial to investigate in vivo the response of UM to imatinib mesylate.


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