Somatic activation of KIT in distinct subtypes of melanoma
This study found KIT mutations and amplifications in a substantial minority of mucosal, acral and chronically sun-damaged skin melanomas but almost never in ordinary skin melanoma, identifying a targetable driver for these rarer subtypes.
Overview
Analysis of 102 primary melanomas from mucosal, acral, chronically sun-damaged and non-sun-damaged sites for KIT copy number and mutations, finding KIT alterations in 39 percent of mucosal, 36 percent of acral and 28 percent of chronically sun-damaged melanomas, and none in non-sun-damaged skin melanomas.
- KIT aberrations in 39 percent of mucosal, 36 percent of acral and 28 percent of chronically sun-damaged melanomas.
- Absent in melanomas on skin without chronic sun damage.
KIT joined BRAF and NRAS as a melanoma driver and became the rationale for imatinib and nilotinib in mucosal and acral melanoma.
- Later series found lower mutation frequencies (about 10 to 15 percent) in mucosal and acral melanoma.
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