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JNCI Journal of the National Cancer Institute 2004 96(12):893-894; doi:10.1093/jnci/djh190
© 2004 by Oxford University Press
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© 2004 Oxford University Press

EDITORIAL

Advancing the Calcium–Colorectal Cancer Hypothesis

Arthur Schatzkin, Ulrike Peters

Affiliation of authors: Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD

Correspondence to: Arthur Schatzkin, MD, DrPH, Nutritional Epidemiology Branch, Executive Plaza South, 6120 Executive Blvd., Rockville, MD 20852 (e-mail: schatzka@mail.nih.gov)

The first 10% of the full text of this article appears below.

Two decades ago, Newmark et al. (1) implicated calcium intake in colorectal carcinogenesis. They hypothesized that calcium ions in the lumen of the large bowel neutralize the toxic effects of free ionized fatty acids and bile acids through the formation of insoluble mineral-fat complexes or soaps. Subsequent experiments (2) showed that calcium could inhibit colon cancer in animals. A particularly influential study (3) demonstrated that calcium supplementation reduced rectal epithelial cell proliferation in humans. Recent studies suggest that luminal calcium directly affects colorectal tumors via the calcium sensing receptor (CASR), which is located in the plasma membrane where it detects extracellular calcium concentration (4); investigation of CASR allelic variants . . . [Full Text of this Article]


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