Study provides direct evidence of the role of telomeres in prostate cancer d...( han those of adjacent normal-appearing ...)

Human tissues from prostate cancer patients, ranging from 47 to 67 years of age, were tested through microscopic examination of prostate tissue sections hybridized with a telomere-specific fluorescent peptide nucleic acid (PNA) probe. These tests revealed markedly reduced telomere signals in HGPIN lesions when compared to either the surrounding stroma (the supporting framework of an organ typically consisting of connective tissue), or to the stroma and epithelia of adjacent normal-appearing glands. Analysis of the telomere signals in a randomly-selected subset of cases revealed statistically significant telomere shortening in luminal cells (cells lining the prostatic ducts) in nine out of the 11 HGPIN lesions (82 percent) when compared to adjacent normal-appearing prostate luminal epithelial cells. The research suggests that the telomeres of PIN lesions are approximately four-fold shorter than their normal counterparts.

Perhaps most interestingly, the telomere shortening in HGPIN lesions was restricted to the luminal epithelial cells, and did not appear to occur within the basal cell compartment (at the base of the prostatic ducts, directly beneath the luminal cells). When compared to the underlying basal cell layer within the same HGPIN lesions, telomere lengths of the HGPIN luminal cells were statistically significantly shorter than the basal cells in all PIN lesions examined. Since basal cells are thought to produce secretory cells (cells that release functionally specialized secretions), it has been assumed that they are the cells that proliferate and undergo physiological transformations. However, these findings suggest that the luminal cells are not the target for potential cancerous transformation.

"We propose that telomeres are stabilized in the subset of PIN lesions that activate telomerase, and that it is these PIN lesions, theoret
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Contact: Aimee Frank
AMF@spectrumscience.com
202-369-1654
American Association for Cancer Research
16-Oct-2002