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Kit Gene in Endometrial Carcinoma: An Immunohistochemical and Mutational Analysis
  1. Ingrid Vandenput, MD*,
  2. Maria Debiec-Rychter, MD,
  3. An Capoen, MD,
  4. Godelieve Verbist, MD, PhD*,
  5. Ignace Vergote, MD, PhD*,
  6. Philippe Moerman, MD, PhD and
  7. Frédéric Amant, MD, PhD*
  1. * Leuven Cancer Institute, Gynecologic Oncology, Departments of
  2. Human Genetics and
  3. Pathology, UZ Gasthuisberg, Katholieke Universiteit Leuven, Belgium.
  1. Address correspondence and reprint requests to Frédéric Amant, MD, PhD, Division of Gynecological Oncology, Department of Obstetrics and Gynecology, University Hospitals Leuven, Herestraat 49, 3000 Leuven, Belgium. E-mail: frederic.amant{at}


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.

  • KIT gene
  • Immunohistochemistry
  • Mutation analysis
  • Endometrial cancer
  • Targeted therapy

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