The CancerWeb Report, What's New In Cancer: October, 1996
Prostate Cancer

• Prostate cancer and vitamin D - It is becoming increasingly more evident that vitamin D, especially the active 1,25-D form and its receptor, play major roles in cancer development. There is evidence suggesting that this general relationship also extends to prostate cancer. Rates for prostate cancer are higher in northerly latitudes, which is compatible with a low exposure to UV, thus leading to reduced synthesis of the vitamin. In addition, the risk of developing this cancer is lower in those with higher serum 1,25-D levels. There are different subtypes of the vitamin D receptor gene. An article in the September 15, 1996 issue of Cancer Research described a study which found that the risk of prostate cancer for men homozygous (both genes the same) for the Bat type of the vitamin D receptor gene, who have higher blood levels of 1,25-D, was one third of that for men homozygous or heterozygous (one gene for baT the other for Bat) for the baT form. Use of 1,25-D supplements as a preventive for prostate cancer could create a problem, because this vitamin plays a major role in calcium metabolism. It might be possible to use some synthetic form of vitamin D with less effect on calcium metabolism as a prostate cancer preventive given to those with the genetic predisposition. (Taylor, Cancer Res 56:4108, 1996)

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• Potential genetic markers for progression of prostate cancer? - Two recent articles raise hope that researchers are beginning to home in on useful markers for prostate cancer that might help distinguish the minority of aggressive, life-threatening tumors from those that pose little or no threat during a patient's lifetime.

  The first was a report from the M.D. Anderson Cancer Center in Houston, Texas, published in the September, 1996 issue of Clinical Cancer Research, which pointed to an abnormality in chromosome 7 as a potential predictor of cancer progression and metastasis. A feature of more aggressive cancers is what is termed their genetic instability, a tendency to show a range of abnormal genetic features or damage. In the study described, these researchers used a fluorescence technique known as FISH to determine the incidence of cells containing three copies (trisomy) of chromosome 7 instead of the usual two, using the unaffected chromosome 9 as a standard. Trisomy of chromosome 7 was not found in most fine needle biopsy samples of normal prostate tissue from 30 prostate cancer patients, and since in those few cases when it occurred (!% or less) it was present almost exclusively in patients with advanced disease, those cells in which it occurred were probably tumor cells. The frequency of trisomy was 6.2% in cancer confined to the prostate (Stage B), 7.1% in tumors with extension outside the prostate (Stage C), and 15.9% for those with pelvic lymph node or seminal vesicle involvement (Stage Csv and D1). Trisomy may be a useful marker of prostate cancer progression and an aid to treatment planning. (Wang, Clin Cancer Res 2:1553, 1996)

  The second article, which in this case involved chromosome 11, was published in the October 1, 1996 issue of Cancer Research by researchers from Johns Hopkins University in Baltimore, Nijmegen University in the Netherlands, and the National Institute of Environmental Health Sciences in Research Triangle Park, North Carolina. They found that production of the protein coded by the KA11 gene, which occurs on chromosome 11 and is considered to be a metastasis-suppressing gene, was reduced or absent in metastatic prostate cancers. The gene was neither damaged nor deleted, but was simply not expressed, a status described as being downregulated. It appeared to be a feature of prostate cancer progression. (Dong, Cancer Res 56:4387, 1996)