PURPOSE: To assess the immunohistochemical profile of the atypical nuclei in leiomyoma with bizarre nuclei and compare with benign and malignant counterparts. METHODS: 26 cases of uterine smooth muscle tumors including 12 leiomyosarcoma(LMS), 10 leiomyoma with bizarre nuclei (LBN) and 4 smooth muscle tumor with uncertain malignant potential (STUMP) were selected using whole tissue sections for this study and analysis. Six cases of ordinary leiomyoma were included as benign control group. All representative section were stained for P53, Ki67, estrogen receptor and progestrone receptor. Analysis was carried out using SPSS 16.0 for windows software. RESULTS: Six out of 12 cases of LMS showed strong and diffuse nuclear staining with p53 antibody (50%). In contrast none of STUMPs and only one case of LBN cases showed focal positive reaction with P53. Percentage of positive cells for ki67 in LMS was 14.92 while only 0.85% of cells in LBNs was labeled with Ki67 proliferative marker. (P<0.001). Regarding steroid hormone receptors a significant loosing trend was found in these receptors from benign toward malignant tumors through LBN and STUMP cases. CONCLUSION: Loss of inhibitory function of wild type P53 gene in leiomyosarcoma is an essential event that discriminate frankly malignant tumors from STUMP and atypical leiomyoma.
PURPOSE: To assess the immunohistochemical profile of the atypical nuclei in leiomyoma with bizarre nuclei and compare with benign and malignant counterparts. METHODS: 26 cases of uterine smooth muscle tumors including 12 leiomyosarcoma(LMS), 10 leiomyoma with bizarre nuclei (LBN) and 4 smooth muscle tumor with uncertain malignant potential (STUMP) were selected using whole tissue sections for this study and analysis. Six cases of ordinary leiomyoma were included as benign control group. All representative section were stained for P53, Ki67, estrogen receptor and progestrone receptor. Analysis was carried out using SPSS 16.0 for windows software. RESULTS: Six out of 12 cases of LMS showed strong and diffuse nuclear staining with p53 antibody (50%). In contrast none of STUMPs and only one case of LBN cases showed focal positive reaction with P53. Percentage of positive cells for ki67 in LMS was 14.92 while only 0.85% of cells in LBNs was labeled with Ki67 proliferative marker. (P<0.001). Regarding steroid hormone receptors a significant loosing trend was found in these receptors from benign toward malignant tumors through LBN and STUMP cases. CONCLUSION: Loss of inhibitory function of wild type P53 gene in leiomyosarcoma is an essential event that discriminate frankly malignant tumors from STUMP and atypical leiomyoma.
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