Can telomere alterations predict biochemical recurrence in prostate adenocarcinoma? A preliminary study.

Telomeres function in human somatic tissues to stabilize chromosome ends. Telomere shortening can be one of the ways that cause chromosomal instability in the pathogenesis of prostatic carcinoma. In the current study, we evaluated telomere length (TL) in normal and malignant prostate tissues, and its association with prognostic factors and with time to biochemical tumor recurrence. Tissue microarrays constructed from paraffin blocks from radical prostatectomy specimens containing 61 randomly selected cases were used. Sections were hybridized with a Cy3-labeled telomere-specific peptide nucleic acid probe. TL, proportional to probe fluorescence intensity, was visually evaluated. Statistical analysis was done to relate TL clinical and pathological prognostic variables. The majority (49/61) of prostate cancers displayed abnormally short telomeres. Univariate analysis revealed inverse correlation between telomere shortening in tumor and Gleason scores (p=0.017). Multivariate analyses pointed to TL as an independent predictor in addition to serum pre-operative PSA for reduced biochemical progression-free survival (p=0.035). Telomere shortening is a common alteration in prostatic adenocarcinoma. Normal or long telomeres are rarely seen and, when present, seem to provide a growth advantage for the tumor as being an advocate for poor differentiation.