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pubmed:abstractText |
High dietary calcium has been shown in epidemiological studies to be a risk factor for prostate cancer, and it has been postulated that this effect is secondary to calcium induced modulation of the vitamin D axis. In this study, we used LPB-Tag transgenic mice on the CD1 background to examine the impact of dietary calcium on prostate tumor progression. CD1-LPB-Tag mice predictably develop autochthonous, hormone-responsive prostate tumors by 3 months of age. Age matched transgenic and non-transgenic littermates were weaned onto high (2%) or low (0.2%) calcium diets and mice were sacrificed at 5, 7, and 9 weeks of age. The entire urogenital complex was excised, weighed, and processed for histology. There was no significant effect of dietary calcium on tumor weight or on the time course of tumor progression, as monitored using a modified Gleason grade (MGS). Serum calcium was maintained in the normal range in mice on the low and high calcium diet throughout the study. Circulating 1,25(OH)(2)D(3) was elevated by low dietary calcium in 5-week-old mice, but not in older animals. In summary, neither development nor progression of prostate tumors in LPB-Tag mice was accelerated by high dietary calcium.
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pubmed:affiliation |
Department of Biological Sciences, University of Notre Dame, 222 Galvin Life Sciences Building, Notre Dame, IN 46556, USA.
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