Study provides direct evidence of the role of telomeres in prostate cancer d...( Boston MA (October 16 2002) Telomere...)

Boston, MA (October 16, 2002) Telomere shortening has been proposed as an early and prevalent marker of prostate cancer process, according to a study presented today at the American Association for Cancer Research's first annual Frontiers in Cancer Prevention Research meeting. Findings of the study provide the first direct evidence that human prostate cancer may progress, in the earliest phase, via chromosomal instability generated by short telomeres, by revealing that telomere shortening is a defining DNA alteration characterizing early prostate cancer lesions.

Telomere shortening may cause significant alterations at the chromosomal level of tumors initiating chromosomal instability and causing progression to a fully malignant state. Telomeres are specialized structures located at the end of chromosomal arms that stabilize and protect chromosomes. In addition, they play a role in preventing cells from reproducing uncontrollably.

"Our study found that short telomeres may represent useful markers for assessing effectiveness in cancer chemoprevention studies," according to Alan Meeker, research fellow and lead investigator of the study which was conducted by researchers at the Brady Urological Institute and Department of Pathology, The Johns Hopkins University School of Medicine. "In addition, if telomere shortening does play a direct, causal role in the cancer process, then it represents an important prevention target in its own right."

In order to test the hypothesis that telomere shortening is an early contributor to human prostate cancer, the researchers developed and validated a new test that allows direct assessment of telomere length in clinical specimens. This study probed telomere lengths in high-grade prostatic intraepithelial neoplasia (HGPIN), the pre-invasive precursor to prostate cancer. Results showed that the telomere lengths of epithelial cells (relating to cellular tissue) within HGPIN lesions were strikingly shorter t
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Contact: Aimee Frank
AMF@spectrumscience.com
202-369-1654
American Association for Cancer Research
16-Oct-2002

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