title: PTEN expression in endometrial biopsies as a marker of progression to endometrial carcinoma.
abstract: Inactivation of PTEN tumor suppressor gene is common in endometrial carcinoma and its precursor, atypical endometrial hyperplasia (EH). We compared PTEN expression via immunohistochemistry in endometrial biopsies diagnosed as EH in 138 cases, who were diagnosed with EH and then endometrial carcinoma at least 1 year later (median, 6 years), and 241 individually matched controls, who were diagnosed with EH but did not progress to carcinoma during equivalent follow-up. We assessed PTEN status (normal versus null) in index biopsies containing EH to estimate the relative risk (RR) of developing endometrial carcinoma up to 25 years later. Analysis of 115 cases and 193 controls with satisfactory assays revealed PTEN-null glands in index biopsies of 44% of cases and 49% of controls [P = 0.85; RR, 1.51; 95% confidence interval (CI), 0.73-3.13]. For predicting progression to carcinoma, PTEN-null status had low sensitivity (44%; 95% CI, 45-54%) and specificity (51%; 95% CI, 44-58%). Among 105 cases with PTEN results for both index biopsy and carcinoma, 16% had a PTEN-null index biopsy, 23% had PTEN-null carcinoma, and 26% had both a PTEN-null index biopsy and carcinoma. Loss of PTEN expression in endometrial biopsies was neither associated with nor a sensitive and specific marker of subsequent progression to endometrial carcinoma.
authors.affiliation: Hormonal and Reproductive Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland, USA. jimlacey@nih.gov
authors.forename: James V
authors.initials: JV
authors.lastname: Lacey
authors.forename: George L
authors.initials: GL
authors.lastname: Mutter
authors.forename: Brigitte M
authors.initials: BM
authors.lastname: Ronnett
authors.forename: Olga B
authors.initials: OB
authors.lastname: Ioffe
authors.forename: Máire A
authors.initials: MA
authors.lastname: Duggan
authors.forename: Brenda B
authors.initials: BB
authors.lastname: Rush
authors.forename: Andrew G
authors.initials: AG
authors.lastname: Glass
authors.forename: Douglas A
authors.initials: DA
authors.lastname: Richesson
authors.forename: Nilanjan
authors.initials: N
authors.lastname: Chatterjee
authors.forename: Bryan
authors.initials: B
authors.lastname: Langholz
authors.forename: Mark E
authors.initials: ME
authors.lastname: Sherman
mesh_terms: D000328:Adult; D000368:Aged; D001706:Biopsy; D002277:Carcinoma / Q000378:metabolism*; D016022:Case-Control Studies; D018450:Disease Progression; D016889:Endometrial Neoplasms / Q000378:metabolism*; D004717:Endometrium / Q000378:metabolism*; D005260:Female; D020869:Gene Expression Profiling; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008875:Middle Aged; D051059:PTEN Phosphohydrolase / Q000096:biosynthesis* / Q000235:genetics*; D012680:Sensitivity and Specificity
chemical_list: D051059:PTEN Phosphohydrolase; C494929:PTEN protein, human