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Telomeric DNA: Marker for human prostate cancer development?

BACKGROUND Telomeres that protect chromosomes at both ends are shortened with each somatic cell division through replication‐dependent sequence loss at DNA termini. The chromosomes with shortened telomeres tend to become unstable, leading to cell death. Due largely to reactivation/upregulation of te...

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Published in:The Prostate 1998-09, Vol.36 (4), p.264-271
Main Authors: Ozen, Mustafa, Imam, S. Ashraf, Datar, Ram H., Multani, Asha S., Narayanan, Ram, Chung, Leland W.K., von Eschenbach, Andrew C., Pathak, Sen
Format: Article
Language:English
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Summary:BACKGROUND Telomeres that protect chromosomes at both ends are shortened with each somatic cell division through replication‐dependent sequence loss at DNA termini. The chromosomes with shortened telomeres tend to become unstable, leading to cell death. Due largely to reactivation/upregulation of telomerase, a ribonucleoprotein that adds nucleotide sequences onto chromosome ends, cancer cells become immortal and neoplastically transformed. METHODS The purpose of the present study was to study three newly established human prostate cancer cell lines and three prostate‐derived fibroblastic cell cultures at different passages for telomeric DNA signal intensity, telomeric restriction fragment length (TRFL), telomerase activity, and spontaneous apoptotic index. RESULTS Compared with the three fibroblastic cell cultures, the three new prostate cancer cell lines showed: 1) telomerase activity, 2) stronger telomeric signals, 3) relatively longer TRFLs, and 4) much lower apoptotic indices. On the other hand, three fibroblastic cell cultures showed: 1) no telomerase activity, 2) weaker telomeric signals, 3) shorter TRFLs (fibroblasts derived from surrounding tissue of prostate tumor showed intermediate TRFLs), and 4) comparatively higher apoptotic indices. CONCLUSIONS Based on these results, we conclude that telomeric DNA signal intensity, TRFL, and telomerase activity can be used to distinguish prostate cancer cells from adjacent fibroblasts. Prostate 36:264–271, 1998. © 1998 Wiley‐Liss, Inc.
ISSN:0270-4137
1097-0045
DOI:10.1002/(SICI)1097-0045(19980901)36:4<264::AID-PROS8>3.0.CO;2-F