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Carcinogenesis Advance Access published online on April 3, 2009
Carcinogenesis, doi:10.1093/carcin/bgp076
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© The Author 2009. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Genetic variation in the vitamin C transporter, SLC23A2, modifies the risk of HPV16-associated head and neck cancer

Alyce A. Chen1,2, Carmen J. Marsit3, Brock C. Christensen3,4, E. Andrés Houseman4, Michael D. McClean5, Judith F. Smith6, Janine T. Bryan6, Marshall R. Posner7, Heather H. Nelson8,9 and Karl T. Kelsey3,4,*

1 The Channing Laboratory, Brigham and Women's Hospital, Boston, MA
2 Biological Sciences in Public Health, Harvard School of Public Health, Boston, MA
3 Department of Pathology and Laboratory Medicine
4 Department of Community Health, Center for Environmental Health and Technology, Brown University, Providence, RI
5 Department of Environmental Health, Boston University School of Public Health, Boston, MA
6 Department of Vaccine Basic Research, Merck and Co., Inc., West Point, PA
7 Head and Neck Oncology Program, Dana-Farber Cancer Institute, Boston, MA
8 Masonic Cancer Center
9 Department of Epidemiology and Community Health, University of Minnesota, Minneapolis, MN

* Corresponding Author: Karl_Kelsey{at}brown.edu, Phone: 401-863-6420, Fax: 401-863-9008

Human papillomavirus type 16 (HPV16) infection is an etiologic factor in a subset of head and neck squamous cell carcinomas (HNSCC). It is unknown if host genetic susceptibility modifies the HPV16-HNSCC association. DNA samples collected as part of a Boston area case control study of HNSCC were genotyped for single nucleotide polymorphisms (SNPs) from the National Cancer Institute's SNP500Cancer database. Analysis of demographic, phenotypic, and genotypic data for 319 HNSCC cases and 495 frequency matched controls was performed using unconditional logistic regression. All reported p-values are two sided. We identified a polymorphism in the sodium-dependent vitamin C transporter SLC23A2 that modifies the risk of HNSCC associated with HPV16 infection. Among those with a wild-type allele at SLC23A2, the risk of HNSCC associated with HPV16- positive serology was 5.0 (95% CI = 3.2 – 7.8). However, among those with a homozygous variant genotype, the risk of HNSCC associated with HPV16 was attenuated (OR = 2.8; 95% CI = 1.2 - 6.2). Further, when we tested whether genotype modified the interaction between citrus exposure, HPV16, and HNSCC we found a dramatically increased risk of HNSCC for those with a wild-type SLC23A2 allele, HPV16-positive serology, and high citrus intake (OR = 7.4; 95% CI = 3.6 - 15.1). These results suggest that SLC23A2 genetic variation alters HPV16-associated HNSCC while also highlighting the important role of citrus exposure in this disease.

Received January 21, 2009; revised March 15, 2009; accepted March 24, 2009.


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