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학술저널
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연세대학교 의과대학 Yonsei Medical Journal Yonsei Medical Journal 제61권 제7호
발행연도
2020.1
수록면
562 - 571 (10page)

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Melanoma, originating from epidermal melanocytes, is a heterogeneous disease that has the highest mortality rate among alltypes of skin cancers. Numerous studies have revealed the cause of this cancer as related to various somatic driver mutations, includingalterations in KIT—a proto-oncogene encoding for a transmembrane receptor tyrosine kinase. Although accounting foronly 3% of all melanomas, mutations in c-KIT are mostly derived from acral, mucosal, and chronically sun-damaged melanomas. As an important factor for cell differentiation, proliferation, and survival, inhibition of c-KIT has been exploited for clinical trialsin advanced melanoma. Here, apart from the molecular background of c-KIT and its cellular functions, we will review the widedistribution of alterations in KIT with a catalogue of more than 40 mutations reported in various articles and case studies. Additionally,we will summarize the association of KIT mutations with clinicopathologic features (age, sex, melanoma subtypes, anatomiclocation, etc.), and the differences of mutation rate among subgroups. Finally, several therapeutic trials of c-KIT inhibitors, includingimatinib, dasatinib, nilotinib, and sunitinib, will be analyzed for their success rates and limitations in advanced melanomatreatment. These not only emphasize c-KIT as an attractive target for personalized melanoma therapy but also propose therequirement for additional investigational studies to develop novel therapeutic trials co-targeting c-KIT and other cytokines suchas members of signaling pathways and immune systems.

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