KIT protein expression and analysis of c-kit gene mutation in adenoid cystic carcinoma

Citation
Va. Holst et al., KIT protein expression and analysis of c-kit gene mutation in adenoid cystic carcinoma, MOD PATHOL, 12(10), 1999, pp. 956-960
Citations number
44
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research Diagnosis & Treatment
Journal title
MODERN PATHOLOGY
ISSN journal
08933952 → ACNP
Volume
12
Issue
10
Year of publication
1999
Pages
956 - 960
Database
ISI
SICI code
0893-3952(199910)12:10<956:KPEAAO>2.0.ZU;2-7
Abstract
The c-kit proto-oncogene encodes a transmembrane receptor tyrosine kinase ( KIT), which is expressed in several normal human tissues, especially mast c ells and interstitial cells of Cajal. Expression of KIT has been noted in s everal types of neoplasms and gene mutation has been shown as a mechanism o f c-kit oncogene activation in some tumors. Recently, a single adnexal aden oid cystic carcinoma (ACC) was reported to demonstrate KIT expression, howe ver, examination of KIT expression or c-kit mutation in ACC of salivary gla nds has not been performed. We examined archival tissue samples from 30 ACC of major and minor salivary glands for KIT protein expression by immunohis tochemistry with a polyclonal antibody and c-kit gene mutation by polymeras e chain reaction amplification and DNA sequencing. KIT protein expression w as noted in 90% of ACCs. An association between the presence of at least 50 % KIT positive neoplastic cells and Grade 3 ACC or a solid growth pattern w as observed (P < .05). KIT expression in normal or nonneoplastic salivary g land tissue was absent. No c-kit juxtamembrane domain (exon 11) or phosphot ransferase domain (exon 17) mutations were found in any of the tumors exami ned. In conclusion, KIT protein expression is correlated with tumor grade o f salivary ACC. However, gene mutation of exon 11 or exon 17 is not a mecha nism of c-kit activation in these neoplasms.