Epidermal Growth Factor Receptor Gene Status by Fluorescence In Situ Hybridization in Malignant, Atypical, and Benign Hidradenomas

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Background:Epidermal growth factor receptor (EGFR) protein overexpression and gene amplification are important prognostic factors in various tumors and EGFR inhibitors are now available as promising chemotherapeutic agents. There is little information in the literature regarding the EGFR protein and gene status in hidradenocarcinomas which has an aggressive biologic course characterized by repeated local recurrences and systemic metastasis. We have previously reported EGFR protein overexpression in malignant, atypical, and benign hidradenomas and would like to further evaluate their gene status by fluorescence in situ hybridization.Methods:Fluorescence in situ hybridization by 2-color probe Vysis LSI EGFR SpectrumOrange/CEP 7 SpectrumGreen Probe (Abbott Molecular) and EGFR immunostain (H11, Dakocytomation) were performed in 15 malignant, 15 atypical, and 7 benign hidradenomas.Results:High polysomy and low trisomy was noted in 1 and 4 hidradenocarcinoma, respectively; however, EGFR overexpression was seen only in 1 low trisomy case. Disomy is noted in the remaining 29 cases (9 hidradenocarcinomas, 15 atypical hidradenomas, and 5 benign hidradenomas). EGFR overexpression was seen in 3/12 (25%) malignant hidradenomas, 7/15 (47%) atypical hidradenomas, and 3/5 (60%) benign hidradenomas; none of these cases demonstrated EGFR gene amplification.Conclusions:Polysomy/trisomy is more frequently seen in hidradenocarcinoma than atypical and benign hidradenomas. The role of EGFR inhibitor therapy in hidradenocarcinoma cases with protein overexpression remains unclear. Lack of correlation between the protein expression and polysomy/gene amplification suggests that molecular mechanisms other than gene amplification play a role in EGFR overexpression in malignant, atypical, and benign hidradenomas.

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