Telomerase Activity And Expression Of Telomerase Components In Prostate Cancer

At some point after the onset of genetic instability caused by telomere shortening, the developing tumor must re-stabilize its telomeres to prevent runaway genetic damage that would ultimately accumulate to lethal levels. Prostate cancers, similar to most other human cancers, typically accomplish this by activating the enzyme telomerase.

Telomerase can be assayed in a number of different ways. Expression of the RNA species encoding either the catalytic protein subunit or the template RNA can be determined by RT-PCR or in situ hybridization techniques, whereas telomerase enzymatic activity can be assayed in tissue lysates using a highly sensitive PCR-based assay (90).

Several studies have assayed telomerase activity in clinical prostate samples, all of which have found detectable activity in tissue lysates from cancerous regions (62,63,90,127-133). The proportion of telomerase positive cases ranges from 47 to 100%, with most reports finding activity in the majority of cases (Table 1). When tested, activity is found less frequently in adjacent normal-appearing regions (no activity in three of five studies) or areas of BPH associated with cancer (10-50% of samples), and, in such cases, the level of activity is typically much less than that found in cancer. Being PCR-based, the telomerase activity assay is highly sensitive, capable of detecting activity as few as 10 cancer cells. Therefore, it remains unknown whether the activity detected in cancer-adjacent areas represents true positivity in normal cells, transformed cells (e.g., PIN), or if it originates

Table 1

Telomerase Activity in Surgically Removed Prostate Tissues''

Table 1

Telomerase Activity in Surgically Removed Prostate Tissues''

Primary

Normal

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