title: GLUT-1 expression in pancreatic neoplasia: implications in pathogenesis, diagnosis, and prognosis.
abstract: OBJECTIVE
  GLUT-1 has been found to have an important role in the upregulation of various cellular pathways and implicated in neoplastic transformation correlating with biological behavior in malignancies. However, literature regarding the significance of GLUT-1 expression in pancreatic neoplasia has been limited and controversial.
  
  
  METHODS
  Immunohistochemical expression of GLUT-1 was tested in a variety of pancreatic neoplasia including ductal adenocarcinomas (DAs), pancreatic intraepithelial neoplasms (PanINs), intraductal papillary mucinous neoplasms (IPMNs), and serous cystadenomas.
  
  
  RESULTS
  There was a progressive increase in the expression of GLUT-1 from low- to higher-grade dysplastic lesions: All higher-grade PanINs/IPMNs (the ones with moderate/high-grade dysplasia) revealed noticeable GLUT-1 expression. Among the 94 DAs analyzed, there were minimal/moderate expression in 46 and significant expression in 24 DAs. However, all 4 clear-cell variants of DAs revealed significant GLUT-1 immunolabeling, as did areas of clear-cell change seen in other DAs. Moreover, all 12 serous cystadenomas expressed significant GLUT-1. GLUT-1 expression was also directly correlated with DA histological grade (P = 0.016) and tumor size (P = 0.03).
  
  
  CONCLUSIONS
  GLUT-1 may give rise to the distinctive clear-cell appearance of these tumors by inducing the accumulation of glycogen in the cytoplasm. Additionally, because GLUT-1 expression was related to histological grade and tumor size of DA, further studies are warranted to investigate the association of GLUT-1 with prognosis and tumor progression.
authors.affiliation: Department of Pathology, New York University, New York, NY, USA.
authors.forename: Olca
authors.initials: O
authors.lastname: Basturk
authors.forename: Rajendra
authors.initials: R
authors.lastname: Singh
authors.forename: Ecmel
authors.initials: E
authors.lastname: Kaygusuz
authors.forename: Serdar
authors.initials: S
authors.lastname: Balci
authors.forename: Nevra
authors.initials: N
authors.lastname: Dursun
authors.forename: Nil
authors.initials: N
authors.lastname: Culhaci
authors.forename: N Volkan
authors.initials: NV
authors.lastname: Adsay
mesh_terms: D014408:Biomarkers, Tumor / Q000032:analysis*; D002278:Carcinoma in Situ / Q000737:chemistry; D021441:Carcinoma, Pancreatic Ductal / Q000737:chemistry; D002291:Carcinoma, Papillary / Q000737:chemistry; D016009:Chi-Square Distribution; D018293:Cystadenoma, Serous / Q000737:chemistry; D051272:Glucose Transporter Type 1 / Q000032:analysis*; D006801:Humans; D007150:Immunohistochemistry; D053208:Kaplan-Meier Estimate; D009361:Neoplasm Invasiveness; D009367:Neoplasm Staging; D018297:Neoplasms, Cystic, Mucinous, and Serous / Q000737:chemistry; D010190:Pancreatic Neoplasms / Q000737:chemistry* / Q000175:diagnosis / Q000401:mortality / Q000473:pathology / Q000628:therapy; D011237:Predictive Value of Tests; D011379:Prognosis; D016016:Proportional Hazards Models; D018570:Risk Assessment; D012307:Risk Factors; D014421:Turkey; D014481:United States; D015854:Up-Regulation
chemical_list: D014408:Biomarkers, Tumor; D051272:Glucose Transporter Type 1; C495677:SLC2A1 protein, human