Assessment of aberrations on chromosome 8 in prostatic atrophy

BJU Int. 2006 Jul;98(1):184-8. doi: 10.1111/j.1464-410X.2006.06233.x.

Abstract

Objective: To systematically examine the genetic alterations on chromosome 8 in prostate epithelia deriving from atrophic areas, and to compare these alterations with those of cells derived from prostatic intraepithelial neoplasia (PIN) and prostate cancer in the same organ.

Material and methods: Tissue microarrays were constructed from 50 patients with histologically different tissues, including normal, PIN, atrophy and cancer lesions. Control samples were obtained from 10 patients who died from causes other than prostate cancer. Multicolour DNA probes for 8p22, centromere 8 and 8q24 were used to detect genetic alterations by fluorescence in situ hybridisation analysis.

Results: Chromosomal alterations were detected on chromosome 8 in all analysed tissues. Including all observed signal patterns, a gradual increase of nuclei with loss of 8p22 was detected in normal (16%), in atrophy (21%), in PIN (25%) and in cancer tissue (31%), and there was gain in 8q24 in normal tissue (10%), in atrophy lesions (19%), in PIN (21%) and in cancer (27%). Generally, in all three lesion types the percentage of cells with 8q24 gain was significantly lower than the percentage of cells with loss of 8p22.

Conclusion: This investigation confirms the presence of severe chromosomal aberrations in the epithelium of the atrophic glands of the prostate. The aberrations are the same those that can be found in PIN and in prostate cancer. These findings confirm the genetic instability of the cells in the atrophic areas of the prostate, which can be a target for further injuries, leading to prostate cancer.

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Atrophy / genetics
  • Chromosome Aberrations*
  • Chromosomes, Human, Pair 8 / genetics*
  • Humans
  • In Situ Hybridization, Fluorescence
  • Male
  • Middle Aged
  • Prostate / pathology*
  • Prostatic Neoplasms / genetics
  • Prostatic Neoplasms / pathology*