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Receptor tyrosine kinases in sinonasal undifferentiated carcinomas—Evaluation for EGFR, c‐KIT, and HER2/neu expression
Author(s) -
Chernock Rebecca D.,
Perry Arie,
Pfeifer John D.,
Holden Joseph A.,
Lewis James S.
Publication year - 2009
Publication title -
head and neck
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.012
H-Index - 127
eISSN - 1097-0347
pISSN - 1043-3074
DOI - 10.1002/hed.21061
Subject(s) - cd117 , immunohistochemistry , fluorescence in situ hybridization , gene duplication , epidermal growth factor receptor , biology , exon , cancer research , tyrosine kinase , pathology , microbiology and biotechnology , receptor tyrosine kinase , in situ hybridization , polysomy , gene , chromosome , receptor , gene expression , medicine , stem cell , cd34 , genetics
Abstract Background. Our objective was to identify the expression of epidermal growth factor receptor (EGFR), c‐KIT (CD117), and HER2/neu in sinonasal undifferentiated carcinoma (SNUC).Methods. Immunohistochemistry for c‐KIT (CD117), EGFR, and HER2/neu was performed on paraffin‐embedded tissue from SNUC cases. A search for activating mutations in c‐kit exons 9, 11, 13, and 17 or gene amplification was undertaken by high‐resolution DNA melting curve analysis and fluorescence in situ hybridization (FISH) for c‐kit and chromosome 4, respectively.Results. By immunohistochemistry, 9 of 11 cases (81.8%) were diffusely (4+) positive for c‐KIT, 3 of 11 cases (27.3%) were positive for EGFR, and none of the cases were positive for HER2/neu. Neither activating mutations nor gene amplification of c‐kit were detected in any of the 8 assessable tumors.Conclusion. c‐KIT is frequently expressed in SNUC. However, the overexpression is not due to activating mutations or gene amplification. © 2009 Wiley Periodicals, Inc. Head Neck, 2009