The use of tyrosine kinase inhibitors (TKIs) has resulted in successful treatm ent of KIT-positive neoplasms. Carcinosarcoma is a very aggressive neoplasm. Co nsequently, c-kit expression may have significant clinical implications for thi s tumor. The purpose of the present study was to assess ckit expression in the c arcinomatous and sarcomatous element of carcinosarcoma to identify if KIT repres ents a therapeutic target for treatment of this neoplasm. Immunohistochemical st aining for c-KIT was performed on paraffin-embedded tissue blocks of 20 consec utive uterine specimens with carcinosarcoma, 40 with endometrial carcinoma, and 12 with atrophic endometrium. Two pathologists assessed the scoring index of sta ining. In the stromal element of carcinosarcoma, no immunohistochemically c-KIT stained cells were observed and in the epithelial element, a low scoring index of staining was present. In endometrial endometrioid carcinoma, the scoring inde x was high in only 15%of the specimens. In the atrophic endometrium, a low scor ing index was seen in all specimens. Our results seem to suggest that c-kit pro bably plays no major role in the pathogenesis of the majority of these tumors wh ile it may be involved in the pathogenesis of some endometrial carcinomas. In vi ew of the multiple molecular targets that are activated by imatinib mesylate, no definitive conclusions can be drawn with regard its effectiveness in carcinosar comas based on the present study. Further studies of c-kit expression in larger series of carcinosarcomas in order to settle the controversial issues with rega rd to frequency of expression, prognostic, and clinical value are warranted. The use of tyrosine kinase inhibitors (TKIs) has resulted in successful treatm ent of KIT-positive neoplasms. Carcinosarcoma is a very aggressive neoplasm. Co n impe with c-kit expression may have significant clinical implications for thi s tumor. The purpose of the present study was to assess ckit expression in the c arcinomatous and sarcomatous element of carcinosarcoma to identify if KIT repres ents a therapeutic target for treatment of this neoplasm. Immunohistochemical st aining for c-KIT was performed on paraffin-embedded tissue blocks of 20 consec utive uterine specimens with carcinosarcoma, 40 with endometrial carcinoma, and 12 with atrophic endometrium. Two pathologists assessed the scoring index of sta ining. In the stromal element of carcinosarcoma, no immunohistochemically c-KIT stained cells were observed and in the epithelial element, a low scoring index of staining was present. In endometrial endometrioid carcinoma, the scoring inde x was high in only 15% of the specimens In the atrophic endometrium, a low scor ing index was seen in all specimens. Our results seem to suggest that c-kit pro bably plays no major role in the pathogenesis of the majority of these tumors wh ile it may be involved in the pathogenesis. of some endometrial carcinomas. In vi ew of the multiple molecular targets that are activated by imatinib mesylate, no definitive conclusions can be drawn with regard its effectiveness in carcinosar comas based on the present study. Further studies of c-kit expression in larger series of carcinosarcomas in order to settle the controversial issues with rega rd to frequency of expression, prognostic, and clinical value are warranted.