OBJECTIVES: The use of tyrosine kinase inhibitors (TKIs) has resulted in successful treatment of KIT-positive neoplasms. Carcinosarcoma is a very aggressive neoplasm. Consequently, c-kit expression may have significant clinical implications for this tumor. The purpose of the present study was to assess c-kit expression in the carcinomatous and sarcomatous element of carcinosarcoma to identify if KIT represents a therapeutic target for treatment of this neoplasm. METHODS: Immunohistochemical staining for c-KIT was performed on paraffin-embedded tissue blocks of 20 consecutive uterine specimens with carcinosarcoma, 40 with endometrial carcinoma, and 12 with atrophic endometrium. Two pathologists assessed the scoring index of staining. RESULTS: 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 index was high in only 15% of the specimens. In the atrophic endometrium, a low scoring index was seen in all specimens. CONCLUSIONS: Our results seem to suggest that c-kit probably plays no major role in the pathogenesis of the majority of these tumors while it may be involved in the pathogenesis of some endometrial carcinomas. In view of the multiple molecular targets that are activated by imatinib mesylate, no definitive conclusions can be drawn with regard its effectiveness in carcinosarcomas based on the present study. Further studies of c-kit expression in larger series of carcinosarcomas in order to settle the controversial issues with regard to frequency of expression, prognostic, and clinical value are warranted.
OBJECTIVES: The use of tyrosine kinase inhibitors (TKIs) has resulted in successful treatment of KIT-positive neoplasms. Carcinosarcoma is a very aggressive neoplasm. Consequently, c-kit expression may have significant clinical implications for this tumor. The purpose of the present study was to assess c-kit expression in the carcinomatous and sarcomatous element of carcinosarcoma to identify if KIT represents a therapeutic target for treatment of this neoplasm. METHODS: Immunohistochemical staining for c-KIT was performed on paraffin-embedded tissue blocks of 20 consecutive uterine specimens with carcinosarcoma, 40 with endometrial carcinoma, and 12 with atrophic endometrium. Two pathologists assessed the scoring index of staining. RESULTS: 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 index was high in only 15% of the specimens. In the atrophic endometrium, a low scoring index was seen in all specimens. CONCLUSIONS: Our results seem to suggest that c-kit probably plays no major role in the pathogenesis of the majority of these tumors while it may be involved in the pathogenesis of some endometrial carcinomas. In view of the multiple molecular targets that are activated by imatinib mesylate, no definitive conclusions can be drawn with regard its effectiveness in carcinosarcomas based on the present study. Further studies of c-kit expression in larger series of carcinosarcomas in order to settle the controversial issues with regard to frequency of expression, prognostic, and clinical value are warranted.