A new tool for the KIT | Nature Reviews Clinical Oncology

An open-label phase II study has recently sought to identify the subtype of patients with melanoma who might respond best to the multi-kinase inhibitor imatinib mesylate. “A subset of

melanomas is characterized by activating alterations in the gene coding for the kinase KIT. We sought to assess whether KIT inhibition in this subset of melanomas could impact tumor

progression,” stated Richard Carvajal, first author of the study.

Out of 295 cases of melanoma enrolled into the study, 51 patients were identified to have KIT mutations or amplifications. These cases were from a cohort of patients with melanoma subtypes

previously shown to be enriched for these types of genetic alterations (from acral, musocal and chronically sun-damaged sites). The identified patients were offered treatment with imatinib

and 28 patients went on to receive the therapy. Two patients had durable complete responses, two had durable partial responses and five had stable disease that lasted for at least 12 weeks,

with two of these lasting for more than 6 months. As Carvajal pointed out, “our study serves as an important proof of concept that inhibition of the protein KIT in patients with advanced

melanoma that are biologically driven by activating mutations in KIT can lead to significant clinical benefit.” Importantly, not all mutations in KIT had the same responses. All six of the

durable responses were observed in patients with L576P or K642E amino acid substitutions, which are the most common KIT alterations in melanoma.

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