Literature DB >> 22357254

Activating c-KIT mutations in a subset of thymic carcinoma and response to different c-KIT inhibitors.

L Schirosi1, N Nannini, D Nicoli, A Cavazza, R Valli, S Buti, L Garagnani, G Sartori, F Calabrese, A Marchetti, F Buttitta, L Felicioni, M Migaldi, F Rea, F Di Chiara, M C Mengoli, G Rossi.   

Abstract

BACKGROUND: To analyze a multi-institutional series of type C thymic carcinomas (TCs) (including neuroendocrine tumors), focusing on the expression and mutations of c-KIT.
MATERIALS AND METHODS: Immunohistochemical expression of c-KIT/CD117, p63, CD5 and neuroendocrine markers, as well as mutational analysis of c-KIT exons 9, 11, 13, 14, 17 by direct sequencing of 48 cases of TCs. Immunohistochemical and molecular data were statistically crossed with clinicopathological features.
RESULTS: Overall, 29 tumors (60%) expressed CD117, 69% were positive for CD5 and 85% (41 cases) for p63. Neuroendocrine markers stained all six atypical carcinoids and five poorly-differentiated thymic squamous cell carcinomas. Overall, six CD117-positive cases (12.5%) showed c-KIT mutation. No mutation was detected in CD117-negative tumors and carcinoids. All the mutations were found in poorly-differentiated thymic squamous cell carcinomas expressing CD117, CD5, p63 and lacking neuroendocrine markers (6 of 12 cases with these features). Mutations involved exon 11 (four cases: V559A, L576P, Y553N, W557R), exon 9 (E490K) and exon 17 (D820E).
CONCLUSIONS: All TCs need an immunohistochemical screening with CD117, while c-KIT mutation analysis is mandatory only in CD117-positive cases, particularly when coexpressing CD5 and p63, lacking neuroendocrine differentiation. The finding of c-KIT mutation can predict efficacy with different c-KIT inhibitors.

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Year:  2012        PMID: 22357254     DOI: 10.1093/annonc/mdr626

Source DB:  PubMed          Journal:  Ann Oncol        ISSN: 0923-7534            Impact factor:   32.976


  24 in total

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