title: Expression of PTEN in mycosis fungoides and correlation with loss of heterozygosity.
abstract: BACKGROUND
  Mycosis fungoides (MF) exhibits a variety of underlying molecular defects including aberrations involving the PTEN tumor suppressor gene. Specifically, loss of heterozygosity of PTEN has been previously demonstrated. We hypothesize that abnormalities of PTEN may result in altered immunohistochemical expression of its protein product.
  
  
  METHODS
  Thirty-six MF specimens were stained with monoclonal antibody against PTEN protein. The percentage of nuclei retaining PTEN expression and the staining intensity was recorded.
  
  
  RESULTS
  Average percentage of lymphoma cells retaining expression of the PTEN protein was 92% within patch-stage lesions, 81.4% in plaque-stage lesions, and 81.1% in tumor-stage lesions. Average intensity of staining for patch-stage lesions was 2.90, 2.50 for plaque lesions and 2.44 for tumor lesions. Cases lacking loss of heterozygozity at PTEN (n = 6) had an average expression of 81% and an average intensity of staining of 2.42. Whereas, cases with loss of heterozygozity at PTEN (n = 6) had an average expression of 75% of cells with an average staining intensity of 2.33.
  
  
  CONCLUSIONS
  The percentage of cells retaining PTEN and staining intensity decrease from patch- to plaque-stage lesions, whereas both parameters show mild diminution in tumor lesions compared with plaque lesions. PTEN expression in a small sample seems to correlate with previous demonstration of loss of heterozygosity at the molecular level. Although a trend for loss of PTEN expression exists with histologic progression of MF, the effect is modest and may not represent the pivotal defect in MF pathogenesis.
authors.affiliation: Department of Pathology, Division of Dermatopathology, University of Arkansas for Medical Sciences, Little Rock, AR, USA. terrence.katona@va.gov
authors.forename: Terrence M
authors.initials: TM
authors.lastname: Katona
authors.forename: Bruce R
authors.initials: BR
authors.lastname: Smoller
authors.forename: Alden L
authors.initials: AL
authors.lastname: Webb
authors.forename: Eyas M
authors.initials: EM
authors.lastname: Hattab
authors.forename: Ahmed
authors.initials: A
authors.lastname: Khalil
authors.forename: Kim M
authors.initials: KM
authors.lastname: Hiatt
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000704:Analysis of Variance; D014408:Biomarkers, Tumor / Q000032:analysis* / Q000235:genetics*; D001706:Biopsy; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D007150:Immunohistochemistry; D019656:Loss of Heterozygosity; D008297:Male; D008875:Middle Aged; D009182:Mycosis Fungoides / Q000201:enzymology* / Q000235:genetics* / Q000473:pathology; D009367:Neoplasm Staging; D051059:PTEN Phosphohydrolase / Q000032:analysis* / Q000235:genetics*; D010641:Phenotype; D012878:Skin Neoplasms / Q000201:enzymology* / Q000235:genetics* / Q000473:pathology
chemical_list: D014408:Biomarkers, Tumor; D051059:PTEN Phosphohydrolase; C494929:PTEN protein, human