PT  - JOURNAL ARTICLE
AU  - Vandenput, Ingrid
AU  - Debiec-Rychter, Maria
AU  - Capoen, An
AU  - Verbist, Godelieve
AU  - Vergote, Ignace
AU  - Moerman, Philippe
AU  - Amant, Frédéric
TI  - <em>Kit</em> Gene in Endometrial Carcinoma: An Immunohistochemical and Mutational Analysis
AID  - 10.1097/IGC.0b013e3182055c94
DP  - 2011 Jan 01
TA  - International Journal of Gynecologic Cancer
PG  - 203--205
VI  - 21
IP  - 2
4099  - http://ijgc.bmj.com/content/21/2/203.short
4100  - http://ijgc.bmj.com/content/21/2/203.full
SO  - Int J Gynecol Cancer2011 Jan 01; 21
AB  - 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 KIT expression 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.