Journal of the National Cancer Institute Advance Access originally published online on July 10, 2007
JNCI Journal of the National Cancer Institute 2007 99(14):1120-1129; doi:10.1093/jnci/djm038
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
© The Author 2007. Published by Oxford University Press.
ARTICLES |
A Nested Case–Control Study of Plasma 25-Hydroxyvitamin D Concentrations and Risk of Colorectal Cancer
Affiliations of authors: Departments of Nutrition (KW, WCW, ELG) and Epidemiology (WCW, ELG), Harvard School of Public Health, Boston, MA; Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA (DF, CSF, WCW, ELG); Division of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA (CSF); Division of Pediatrics, Medical University of South Carolina, Charleston, SC (BWH)
Correspondence to: Kana Wu, MD, PhD, Department of Nutrition, Harvard School of Public Health, 665 Huntington Ave, Bldg 2, Boston, MA 02115 (e-mail: kana.wu{at}channing.harvard.edu).
Background: Low vitamin D status has long been implicated in colorectal carcinogenesis. We investigated this relationship in a nested case–control study within the Health Professionals Follow-up Study (HPFS), a large ongoing study of male health professionals living in the United States.
Methods: Between 1993 and 2002, 179 colorectal cancer patients were diagnosed and matched to 356 control subjects by age and by month and year of blood collection. Results were also pooled with previously published results from the Nurses’ Health Study (NHS) cohort, a large female cohort. Conditional logistic regression was used to analyze the association between plasma 25-hydroxyvitamin D [25(OH)D] and colorectal cancer, and pooled estimates were calculated using the method of DerSimonian and Laird. All statistical tests were two-sided.
Results: In the HPFS, we observed a non–statistically significant inverse association between higher plasma 25(OH)D concentration and risk of colorectal cancer and a statistically significant inverse association for colon cancer (highest versus lowest quintile: odds ratio [OR] = 0.46, 95% confidence interval [CI] = 0.24 to 0.89; Ptrend = .005). After pooling the results from the HPFS and NHS, higher plasma 25(OH)D concentrations were statistically significantly associated with decreased risks of both colorectal cancer (highest versus lowest quintile, OR = 0.66, 95% CI = 0.42 to 1.05; Ptrend = .01) and colon cancer (highest versus lowest quintile, OR = 0.54, 95% CI = 0.34 to 0.86; Ptrend = .002). Inverse associations with plasma 25(OH)D concentration did not differ by location of colon cancer (proximal versus distal), but the number of patients was small and none of the associations was statistically significant. Opposite relationships between plasma 25(OH)D levels and risk of rectal cancers were found among men (positive) and women (inverse).
Conclusion: Our data provide additional support for the inverse association between vitamin D and colorectal and, in particular, colon cancer risk.
| CONTEXT AND CAVEATS Prior knowledge A possible association has been noted between low vitamin D status and colorectal carcinogenesis. Study design Nested case–control study of plasma vitamin D, measured as 25(OH)D, and risk of colorectal cancer among male participants in the Health Professionals Follow-up Study (HPFS). Pooled analyses were also performed with previous results from the Nurses’ Health Study. Contribution Higher plasma 25(OH)D concentrations were associated with a decreased risk of colon cancer among participants in the HPFS and with decreased risks of colon and colorectal cancer in the pooled analysis. Implications There is an inverse association between vitamin D and risk for colon cancer in these study populations. Limitations They study follow-up period was only 8 years in the HPFS and 11 years in the Nurses’ Health Study. Plasma vitamin D concentrations were determined from blood samples that were provided at only one time point.
|
Manuscript received February 7, 2007; revised May 18, 2007; accepted May 31, 2007.
Related Article in JNCI
CiteULike 
Connotea 
Del.icio.us What's this?
J Natl Cancer Inst 2007 99: 1057.
This article has been cited by other articles:
|
|
 |
|
  Y. Wang, E. J. Jacobs, M. L. McCullough, C. Rodriguez, M. J. Thun, E. E. Calle, and W. D. Flanders Comparing Methods for Accounting for Seasonal Variability in a Biomarker When Only a Single Sample Is Available: Insights From Simulations Based on Serum 25-Hydroxyvitamin D Am. J. Epidemiol., July 1, 2009; 170(1): 88 - 94. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. J. Goodwin Vitamin D in Cancer Patients: Above All, Do No Harm J. Clin. Oncol., May 1, 2009; 27(13): 2117 - 2119. [Full Text] [PDF]
|
|
|
|
 |
|
 R. Z. Stolzenberg-Solomon, R. B. Hayes, R. L. Horst, K. E. Anderson, B. W. Hollis, and D. T. Silverman Serum Vitamin D and Risk of Pancreatic Cancer in the Prostate, Lung, Colorectal, and Ovarian Screening Trial Cancer Res., February 15, 2009; 69(4): 1439 - 1447. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Ogino, K. Nosho, G. J. Kirkner, T. Kawasaki, A. T. Chan, E. S. Schernhammer, E. L. Giovannucci, and C. S. Fuchs A Cohort Study of Tumoral LINE-1 Hypomethylation and Prognosis in Colon Cancer J Natl Cancer Inst, December 3, 2008; 100(23): 1734 - 1738. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Ishihara, M. Inoue, M. Iwasaki, S. Sasazuki, and S. Tsugane Dietary calcium, vitamin D, and the risk of colorectal cancer Am. J. Clinical Nutrition, December 1, 2008; 88(6): 1576 - 1583. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Ordonez-Moran, M. J. Larriba, H. G. Palmer, R. A. Valero, A. Barbachano, M. Dunach, A. G. de Herreros, C. Villalobos, M. T. Berciano, M. Lafarga, et al. RhoA-ROCK and p38MAPK-MSK1 mediate vitamin D effects on gene expression, phenotype, and Wnt pathway in colon cancer cells J. Cell Biol., November 17, 2008; 183(4): 697 - 710. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Hansdottir, M. M. Monick, S. L. Hinde, N. Lovan, D. C. Look, and G. W. Hunninghake Respiratory Epithelial Cells Convert Inactive Vitamin D to Its Active Form: Potential Effects on Host Defense J. Immunol., November 15, 2008; 181(10): 7090 - 7099. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Y. Wei, C. F. Garland, E. D. Gorham, S. B. Mohr, and E. Giovannucci Vitamin D and Prevention of Colorectal Adenoma: A Meta-analysis Cancer Epidemiol. Biomarkers Prev., November 1, 2008; 17(11): 2958 - 2969. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Bouillon, G. Carmeliet, L. Verlinden, E. van Etten, A. Verstuyf, H. F. Luderer, L. Lieben, C. Mathieu, and M. Demay Vitamin D and Human Health: Lessons from Vitamin D Receptor Null Mice Endocr. Rev., October 1, 2008; 29(6): 726 - 776. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. M. Ochs-Balcom, M. S. Cicek, C. L. Thompson, T. C. Tucker, R. C. Elston, S. J.Plummer, G. Casey, and L. Li Association of vitamin D receptor gene variants, adiposity and colon cancer Carcinogenesis, September 1, 2008; 29(9): 1788 - 1793. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Ng, J. A. Meyerhardt, K. Wu, D. Feskanich, B. W. Hollis, E. L. Giovannucci, and C. S. Fuchs Circulating 25-Hydroxyvitamin D Levels and Survival in Patients With Colorectal Cancer J. Clin. Oncol., June 20, 2008; 26(18): 2984 - 2991. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
I. Soerjomataram, W. J. Louwman, V. E. P. P. Lemmens, J. W. W. Coebergh, and E. de Vries Are Patients with Skin Cancer at Lower Risk of Developing Colorectal or Breast Cancer? Am. J. Epidemiol., June 15, 2008; 167(12): 1421 - 1429. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. D. Davis and J. T. Dwyer The "Sunshine Vitamin": Benefits Beyond Bone? J Natl Cancer Inst, November 7, 2007; 99(21): 1563 - 1565. [Full Text] [PDF]
|
|