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Biomarker Spots Which Lesions Likely to Progress to Prostate Cancer

May 2 (HealthDay News) -- Spanish researchers report they may have found a way to tell which suspicious prostate lesions are likely to develop into cancer.

The findings, published in the May 1 issue of Clinical Cancer Research, show a link between high-grade prostatic intraepithelial neoplasia (HG-PIN) lesions and the PTOV1 gene. The more PTOV1 the lesion expresses, the more likely cancer will develop. The report also backs the reverse -- that the lack of PTOV1 means a reduced risk of prostate cancer.

PTOV1 is a protein that researchers don't fully understand the function of, but they have previously found too much of it appears to promote the spread of cancer cells.

If subsequent studies confirm PTOV1 as a biomarker for prostate cancer, it could help men with the lesions avoid repeated needle biopsies.

"Those patients with a high PTOV1 score should undergo an immediate repeat biopsy," study author Rosanna Paciucci, a researcher at the Vall d'Hebron Hospital Research Institute in Barcelona, said in a prepared statement. But those with low PTOVI may not need to receive future "annoying and useless" biopsies, she said. "We estimate that we can save 40 percent of unnecessary biopsies -- those that are repetitively negative and contain HG-PIN lesions that do not develop into cancer."

HG-PIN, while present in most cancerous prostates, is a pre-malignant lesion and, given its association with other cancers, it is often repeatedly biopsied when found. Past studies have put the average risk of cancer being diagnosed in a HG-PIN biopsy at between 20 percent and 30 percent, the researchers said. However, none of these studies were to tell which lesions would progress to cancer, the researchers say.

Paciucci cautioned that her team's results need to be confirmed through a larger study group. "From this validation, we can expect to improve the current rate of early detection of cancer," she said.


SOURCE: American Association for Cancer Research, news release, May 1, 2008

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