Abstract
Abstract Background: Uterine leiomyoma (ULM) and leiomyosarcoma (ULMS) are smooth muscle tumors with distinct clinical behavior that can cause infertility and even lead to death. Little is known about the factors that influence these tumors biology. Identification of new molecular markers can help in the differential diagnosis between ULM from low grade ULMS. It was demonstrated that activation of the Sonic Hedgehog (SHH) signaling pathway is related to the development of several tumors, through its activity in the cell proliferation and differentiation. Here, we investigated the protein expression profile of SHH, PTCH1, SMO and GLI1 both ULM (including non-typical leiomyomas) and ULMS. Methods: We selected 57 samples of ULMS and 30 samples of ULM (10 samples non-typical - ULMA). All tissues were used in TMA construction. Immunohistochemistry reaction was performed using monoclonal antibody against SHH (1:50), PTCH (1:100), SMO (1:100) and GLI-1 (1:200) using sodium citrate pH 6,0 in pressure cooker. Results were evaluated by Aperio® automated method. Results: Our preliminary data showed similar protein profile between the leiomyosarcoma and non-typical leiomyoma. GLI 1 and PTCH showed higher expression compared to leiomyoma and myometrium (p<0.05). SMO, and SHH showed higher expression only in leiomyossarcomas (p<0.05). Conclusions: Ours preliminary results showed that expression of Sonic Hedgehog pathway members might play an important role in uterine smooth tumors, since ULMS showed higher levels of these proteins. However, the role of these proteins interactions must be clarified. Citation Format: Natalia Garcia, Faila C. Souza, Nilo Bozzini, Glauco Baiocchi, Isabela W. Cunha, Fernando A. Soares, Edmund C. Baracat, Kátia C. Carvalho. SHH pathway in uterine mesenchymal tumors. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2241. doi:10.1158/1538-7445.AM2014-2241
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