{"paper_id":"02680996-c989-4f81-82ee-de40ad73b2f4","body_text":"C-Kit Immunoreactivity in Endometrial Adenocarcinomas and Its Clinicopathologic Significance\n- Janice V. Scobie\n- Geza Acs\n- Christina A. Bandera\n- Stephanie V. Blank\n- James E. Wheeler\n- Teresa L. Pasha\n- Marilyn Salscheider\n- Paul J. Zhang\nSummary:\nThe proto-oncogene c-kit is a transmembrane–tyrosine-kinase receptor that is structurally related to the platelet-derived growth-factor receptor (PDGFR) and is involved in cell differentiation. C-kit has been found to be expressed in certain solid tumors and may play a role in their tumorigenesis. Recently, a tyrosine-kinase inhibitor specific for the PDGFR family, bcr-abl, and c-kit (STI571) has been reported to have therapeutic effects in tumors expressing the aberrant forms or high quantities of target proteins. Expression of c-kit has not been well evaluated in endometrial adenocarcinomas. In this study, c-kit immunoreactivity was evaluated on paraffin sections of 72 endometrial adenocarcinomas (57 endometrioid, 10 serous, and 5 clear cell) with a polyclonal antibody. Immunoreactivity of c-kit was analyzed semiquantitatively and correlated with various clinicopathologic factors. Cytoplasmic c-kit immunoreactivity was detected in 42 (58%) tumors. Thirty-four (60%) endometrioid, 8 (80%) serous, and 0 of the 5 clear-cell adenocarcinomas were c-kit positive. There was a significant correlation between c-kit positivity and the depth of myometrial invasion. Patients with c–kit-positive endometrial adenocarcinomas more frequently had metastases and shorter disease-free survival. Expression of c-kit may be a potentially adverse prognostic feature in endometrial adenocarcinoma. Patients with c–kit-positive advanced endometrial adenocarcinoma might benefit from tyrosine–kinase-inhibitor therapy.","source_license":"CC0","license_restricted":false}