Research: EKMAN and colleagues,

Listed in Issue 45

Abstract

EKMAN and colleagues, Department of Urology, Karolinska Hospital, Stockholm, Sweden write that genetic polymorphisms and expression of steroid receptors may explain why some individuals are more at risk of developing prostate cancer .

Background

Certain risk factors discussed are androgen stimulation and vitamins A and D deficiencies. Long CAG-repeats in exon 1 of the androgen receptor (AR) gene on the X chromosome appear to have a protective role against androgen overstimulation. Also, long vitamin D receptor alleles in the poly-A tract may prevent vitamin D stimulation.

Methodology

Blood samples were taken from 59 Swedish patients with sporadic prostate cancers, 59 with hereditary prostate cancer and from 34 Japanese prostate cancer patients, who were compared with benign controls. The tissue specimens from 37 Swedish and 23 Japanese prostate cancer patients with matching blood samples were investigated using immunohistochemical techniques.

Results

The number of CAG-repeats was identical in sporadic and hereditary prostate cancer patients; however the repeats were significantly shorter than in benign controls. Benign Japanese controls were similar to Swedish controls, but Japanese prostate cancers had longer repeats than did the controls. Both the vitamin D and A receptor staining was stronger in Japanese than in Swedish prostate cancer specimens. Prostate cancer occurs about 5 years later in Japanese compared with Swedish men.

Conclusion

Differing lengths of CAG-repeats of the androgen receptor cant fully explain racial differences in clinical prostate cancer incidence. A larger content of vitamin A and D receptors may be linked to a delayed onset of clinical prostate cancer in Japanese men .

References

Ekman P et al. Links between genetic and environmental factors and prostate cancer risk. Prostate 39(4): 262-8. 1 Jun 1999.

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