title: Organ-wide telomeric status in diseased and disease-free prostatic tissues.
abstract: BACKGROUND
  Telomere attrition occurs early in the development of prostatic adenocarcinoma. However, little is known about either telomere status in benign prostatic hyperplasia (BPH), or the spatial and organ-wide distribution of potential telomere aberrations throughout all areas of prostatic glands affected by cancer or BPH.
  
  
  METHODS
  Slot blot titration assay was used to determine telomere DNA content (TC), a proxy for telomere length, in macrodissected tissue consisting of 54 normal samples from 5 disease-free prostates, 128 BPH samples from 4 non-cancerous prostates, and 45 tumor, 73 BPH, and 4 prostatic intraepithelial neoplasia (PIN) samples from 5 cancerous prostates.
  
  
  RESULTS
  Compared to TC in normal prostate samples (n = 54; TC mean = 0.98), tumor samples displayed telomere attrition (n = 45; TC mean = 0.67). TC in PIN samples was similar to tumors. TC in BPH samples from cancerous prostates was similar to TC in tumors and also displayed telomere shortening (n = 73; TC mean = 0.76), whereas BPH samples from non-cancerous prostates displayed longer telomeres (n = 128; TC mean = 1.06). In prostates affected by adenocarcinoma, areas of potential telomere attrition occurred in histologically normal tissues through the entire gland. However, three-dimensional zoning revealed a pattern of increasing TC as a function of distance from the primary (index) tumor.
  
  
  CONCLUSIONS
  Spatial distributions of TC in prostate specimens indicate a complex "field effect" with varying contributions from both cancer and BPH. The observation that telomere length variations occur in fields of histologically normal tissues surrounding the tumor is of clinical importance, as it may have implications for the diagnosis and focal therapy of prostate cancer.
authors.affiliation: Department of Biochemistry and Molecular Biology, University of New Mexico School of Medicine, Albuquerque, New Mexico 87131, USA.
authors.forename: Christopher M
authors.initials: CM
authors.lastname: Heaphy
authors.forename: Trisha M
authors.initials: TM
authors.lastname: Fleet
authors.forename: Eric G
authors.initials: EG
authors.lastname: Treat
authors.forename: Sang-Joon
authors.initials: SJ
authors.lastname: Lee
authors.forename: Anthony Y
authors.initials: AY
authors.lastname: Smith
authors.forename: Michael S
authors.initials: MS
authors.lastname: Davis
authors.forename: Jeffrey K
authors.initials: JK
authors.lastname: Griffith
authors.forename: Edgar G
authors.initials: EG
authors.lastname: Fischer
authors.forename: Marco
authors.initials: M
authors.lastname: Bisoffi
mesh_terms: D000230:Adenocarcinoma / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D006801:Humans; D008297:Male; D008875:Middle Aged; D011467:Prostate / Q000378:metabolism / Q000473:pathology*; D011470:Prostatic Hyperplasia / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D011471:Prostatic Neoplasms / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D016615:Telomere / Q000378:metabolism / Q000473:pathology*