The study presented by Dr. Alan Meeker, of Johns Hopkins University of Medicine at the annual meeting of the American Association for Cancer Research revealed that telomere shortening is a defining DNA alteration characterizing early prostate cancer lesions.

"Our study found that short telomeres may represent useful markers for assessing effectiveness in cancer chemoprevention studies," Meeker said in a prepared statement. "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."

Chromosomes contain all the genetic material in a cell and in some phases of the cell cycle form x-like structures of tightly wound DNA. Telomeres are special sequences of DNA located at the end of chromosomal arms that stabilize and protect chromosomes. In addition, they play a role in preventing cells from reproducing uncontrollably.

Cells dividing normally stop dividing when the telomeres shorten to a certain, pre-determined length; this action is thought to be a normal anti-tumor mechanism present in long-lived organisms.

Cancer cells, however, achieve "immortality" or a state of continuous cell division when the normal shortening of telomeres is counter-balanced by activation of the enzyme telomerase, which functions to maintain the lengths of telomeres. This enzyme activity has been detected in 85 percent of all cancer cells.

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.

Human tissues from prostate cancer patients, ranging from 47 to 67 years of age, were tested through microscopic examination of prostate tissue sections treated with a telomere-specific fluorescent marker. The brighter the fluorescence shows under examination the longer the telomeres.

This study probed telomere lengths in high-grade precancerous prostate lesions. Results showed that the telomere lengths of epithelial cells, which make up the membrane covering the prostate, within these lesions were strikingly shorter than those of adjacent normal-appearing epithelial cells in 93 percent of lesions examined.

These tests revealed markedly reduced telomeres in the cells of the lesions when compared to the surrounding normal cells. Analysis of the telomeres in a randomly-selected subset of cases revealed the telomeres of these lesions are approximately four-fold shorter than their normal counterparts.

Perhaps most interestingly, the telomere shortening in the high-grade lesions was restricted to the cells lining the prostate ducts and did not appear to occur within the cells at the base of the prostatic ducts.

If further research proves the method the researchers developed to examine telomere length to be reliable it might also be adapted to detect other cancer types.

"We are currently testing the telomere lengths in several other epithelial cancer precursor lesions to determine whether this phenomenon of early telomere shortening is widespread in other cancers," said Meeker.

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