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Title: Expression of Glut-1 in Normal Endometrium and Endometrial Lesions: Analysis of 336 Cases. Author: Němejcová K, Rosmusová J, Bártů M, Důra M, Tichá I, Dundr P. Journal: Int J Surg Pathol; 2017 Aug; 25(5):389-396. PubMed ID: 28381136. Abstract: BACKGROUND: Glucose transporter-1 (Glut-1) is a membrane glycoprotein that is, together with other glucose transporters, responsible for the regulation of glucose uptake. An increased expression of this protein seems to be a general feature of several malignant tumors that are able to reprogram their metabolism and switch from oxidative phosphorylation to aerobic glycolysis. METHODS: We performed comprehensive immunohistochemical analysis of Glut-1 expression in 336 endometrial samples, including tumors, nontumor lesions, and normal tissues. RESULTS: Expression of Glut-1 was found in 87% of endometrioid carcinomas (160/184 cases), 100% of serous carcinomas (29/29 cases), 100% of clear cell carcinomas (17/17 cases), 50% of polyps with atypical hyperplasia (8/16 cases), 12.5% of polyps with non-atypical hyperplasia (3/24 cases), 77% of hyperplasias with atypias (10/13 cases), 9% of hyperplasias without atypias (1/11 cases), 87% of secretory endometrium samples (13/15 cases), and in none of the nonsecretory endometrium samples (0/27 cases). In endometrioid carcinomas, Glut-1 was expressed in a marked geographical pattern. In nontumor lesions, its expression was more common in atypical hyperplasia and polyps with atypical hyperplasia compared with polyps with non-atypical hyperplasia and hyperplasias without atypia ( P = .00032). CONCLUSION: Our study confirms the high expression of Glut-1 not only in endometrioid carcinomas but also in other carcinomas of endometrium including clear cell and serous types. Glut-1 expression can be used as a surrogate marker in differential diagnosis between hyperplasia with and without atypia. Because of common Glut-1 expression in malignant tumors, therapeutic strategies influencing this protein or its signaling pathways can be beneficial.[Abstract] [Full Text] [Related] [New Search]