Kit gene in endometrial carcinoma: An immunohistochemical and mutational analysis

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Abstract

Objective: Because the outcome of recurrent disease of endometrial carcinoma is cumbersome, the development of target treatment strategies is critical. We evaluated KIT, a receptor tyrosine kinase, to determine a potential role for imatinib mesylate in the treatment of endometrial carcinoma. Materials and Methods: Immunohistochemical analysis for KIT expression was performed on paraffin sections from 45 patients: 30 primary and 15 recurrent tumors. Fifteen primary cases were available for mutation analysis. Results: Histopathological distribution of paraffin-embedded tissue was as follows: 30 type I and 15 type II endometrial carcinoma. Histopathological distribution of fresh-frozen tissue was as follows: 8 type I and 7 type II. Cases did not show KITexpression or mutations in mutational hotspot exons of KIT gene. Conclusions: On the basis of the absence of KIT expression or mutations, endometrial carcinoma is unlikely to respond to imatinib mesylate. © 2011 by IGCS and ESGO.

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Vandenput, I., Debiec-Rychter, M., Capoen, A., Verbist, G., Vergote, I., Moerman, P., & Amant, F. (2011). Kit gene in endometrial carcinoma: An immunohistochemical and mutational analysis. International Journal of Gynecological Cancer, 21(2), 203–205. https://doi.org/10.1097/IGC.0b013e3182055c94

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