title: Expression of glucose transporter-1 in cervical cancer and its precursors.
abstract: OBJECTIVE
  Increased glucose uptake and utilization is a known phenomenon exhibited by malignant cells. Overexpression of the glucose transporter protein family is thought to be the principal mechanism by which these cells achieve up-regulation. Our purpose is to determine glucose transporter-1 (GLUT 1) expression in squamous carcinoma of the cervix and precursor lesions.
  
  
  METHODS
  Archival histologic sections were obtained from 31 cases of invasive squamous cell carcinoma (SCC) of the uterine cervix, 15 cases of high-grade cervical intraepithelial neoplasia, 5 cases of low-grade, and 9 normal cervices. Immunohistochemistry for GLUT 1 protein was performed using polyclonal GLUT 1 antibody (Dako, Carpinteria, CA) and the labeled streptavidin-biotin procedure.
  
  
  RESULTS
  Compared to the internal control, the pattern of staining varied from weak (1+) to strong (3+) reactions. In normal cervix, 1+ GLUT 1 staining was seen in the basal cells of the squamous epithelium. All 31 (100%) cases of SCC were positive for GLUT 1. Positive reactions seemed more intense in tumor cells that were farther away from the stromal blood supply. There was a correlation between intensity of reaction for GLUT 1 and histologic grade of tumor (P = 0.0027) and with progression from normal or dysplastic lesions to invasive cancer (P = 0.0001). Intensity was a predictor of the presence of poorly differentiated tumor type. Low-grade CIN staining was seen in less than one-third of the epithelium, while in high-grade lesions the reaction was present in over one-half of the epithelium.
  
  
  CONCLUSIONS
  GLUT 1 is overexpressed in cervical carcinoma. The process appears to be related to grade of tumor but not to the progression from preneoplastic lesions. The results suggest that GLUT 1 overexpression is a late phenomenon in cellular transformation. Furthermore, the possible relation of expression to tumor blood supply suggests that the malignant cells may have an adaptive environmental ability to compensate for a compromised microenvironment.
authors.affiliation: Department of Obstetrics and Gynecology, University of Miami School of Medicine/Jackson Memorial Medical Center, Florida 33136, USA. lmendez@med.miami.edu
authors.forename: Luis E
authors.initials: LE
authors.lastname: Mendez
authors.forename: Natalina
authors.initials: N
authors.lastname: Manci
authors.forename: Guilherme
authors.initials: G
authors.lastname: Cantuaria
authors.forename: Orlando
authors.initials: O
authors.lastname: Gomez-Marin
authors.forename: Manuel
authors.initials: M
authors.lastname: Penalver
authors.forename: Paul
authors.initials: P
authors.lastname: Braunschweiger
authors.forename: Mehrdad
authors.initials: M
authors.lastname: Nadji
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D018450:Disease Progression; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D051272:Glucose Transporter Type 1; D006801:Humans; D007150:Immunohistochemistry; D008875:Middle Aged; D009004:Monosaccharide Transport Proteins / Q000032:analysis* / Q000276:immunology; D009361:Neoplasm Invasiveness; D015854:Up-Regulation; D002583:Uterine Cervical Neoplasms / Q000737:chemistry*; D002578:Uterine Cervical Dysplasia / Q000737:chemistry*
chemical_list: D051272:Glucose Transporter Type 1; D009004:Monosaccharide Transport Proteins; C495677:SLC2A1 protein, human