Affordable Access

deepdyve-link
Publisher Website

Plasma 25-hydroxyvitamin D and colorectal cancer risk according to tumour immunity status.

Authors
  • Song, Mingyang1, 2
  • Nishihara, Reiko1, 3
  • Wang, Molin2
  • Chan, Andrew T4, 5
  • Qian, Zhi Rong3
  • Inamura, Kentaro3, 6
  • Zhang, Xuehong5
  • Ng, Kimmie3
  • Kim, Sun A3
  • Mima, Kosuke3
  • Sukawa, Yasutaka3
  • Nosho, Katsuhiko7
  • Fuchs, Charles S3, 5
  • Giovannucci, Edward L1, 2, 5
  • Wu, Kana1
  • Ogino, Shuji2, 3, 5, 8
  • 1 Department of Nutrition, Harvard School of Public Health, Boston, MA, United States. , (United States)
  • 2 Department of Epidemiology, Harvard School of Public Health, Boston, MA, United States. , (United States)
  • 3 Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA, United States. , (United States)
  • 4 Division of Gastroenterology, Massachusetts General Hospital, Boston, MA, United States. , (United States)
  • 5 Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, and Harvard Medical School, Boston, MA, United States. , (United States)
  • 6 Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD, United States. , (United States)
  • 7 Department of Gastroenterology, Rheumatology and Clinical Immunology, Sapporo Medical University School of Medicine, Sapporo, Japan. , (Japan)
  • 8 Department of Pathology, Brigham and Women's Hospital, and Harvard Medical School, Boston, MA, United States. , (United States)
Type
Published Article
Journal
Gut
Publisher
BMJ
Publication Date
Feb 01, 2016
Volume
65
Issue
2
Pages
296–304
Identifiers
DOI: 10.1136/gutjnl-2014-308852
PMID: 25591978
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Evidence suggests protective effects of vitamin D and antitumour immunity on colorectal cancer risk. Immune cells in tumour microenvironment can convert 25-hydroxyvitamin D [25(OH)D] to bioactive 1α,25-dihydroxyvitamin D3, which influences neoplastic and immune cells as an autocrine and paracrine factor. Thus, we hypothesised that the inverse association between vitamin D and colorectal cancer risk might be stronger for cancers with high-level immune response than those with low-level immune response. We designed a nested case-control study (318 rectal and colon carcinoma cases and 624 matched controls) within the Nurses' Health Study and Health Professionals Follow-up Study using molecular pathological epidemiology database. Multivariable conditional logistic regression was used to assess the association of plasma 25(OH)D with tumour subtypes according to the degree of lymphocytic reaction, tumour-infiltrating T cells (CD3+, CD8+, CD45RO+ (PTPRC) and FOXP3+ cells), microsatellite instability or CpG island methylator phenotype. The association of plasma 25(OH)D with colorectal carcinoma differed by the degree of intratumoural periglandular reaction (p for heterogeneity=0.001); high 25(OH)D was associated with lower risk of tumour with high-level reaction (comparing the highest versus lowest tertile: OR 0.10; 95% CI 0.03 to 0.35; p for trend<0.001), but not risk of tumour with lower-level reaction (p for trend>0.50). A statistically non-significant difference was observed for the associations of 25(OH)D with tumour subtypes according to CD3+ T cell density (p for heterogeneity=0.03; adjusted statistical significance level of α=0.006). High plasma 25(OH)D level is associated with lower risk of colorectal cancer with intense immune reaction, supporting a role of vitamin D in cancer immunoprevention through tumour-host interaction. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/

Report this publication

Statistics

Seen <100 times