Journal Article

Association of hydroxyprostaglandin dehydrogenase 15-(NAD) (<i>HPGD</i>) variants and colorectal cancer risk

Bernd Frank, Birgit Hoeft, Michael Hoffmeister, Jakob Linseisen, Lutz P. Breitling, Jenny Chang-Claude, Hermann Brenner and Alexandra Nieters

in Carcinogenesis

Volume 32, issue 2, pages 190-196
Published in print February 2011 | ISSN: 0143-3334
Published online November 2010 | e-ISSN: 1460-2180 | DOI:
Association of hydroxyprostaglandin dehydrogenase 15-(NAD) (HPGD) variants and colorectal cancer risk

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A recent study examined associations of tagging single nucleotide polymorphisms (tagSNPs) in 43 fatty acid metabolism-related genes and risk of colorectal cancer (CRC), showing rs8752, rs2612656 and a haplotype [comprising both of the single nucleotide polymorphisms (SNPs)] in the hydroxyprostaglandin dehydrogenase 15-(NAD) (HPGD) gene to be positively associated with CRC risk. In the present study, we attempted to replicate these single marker and haplotype associations, using 1795 CRC cases and 1805 controls from the German Darmkrebs: Chancen der Verhütung durch Screening study (DACHS). In addition to rs8752 and rs2612656, HPGD tagSNPs rs9312555, rs17360144 and rs7349744 were genotyped for haplotype analyses. Except for a marginally significant inverse association of HPGD rs8752 with CRC risk [odds ratio (OR) = 0.85; 95% confidence interval (CI) = 0.74, 0.98; P = 0.03], none of the analyzed tagSNPs showed any association with CRC. Subset analyses for colon and rectal cancers yielded similar, yet non-significant risk estimates at all five loci. Also, none of the haplotypes was found to be associated with CRC, colon or rectal cancers. However, rs8752 was significantly associated with a decreased risk of CRC among individuals with a body mass index < 30 (OR = 0.82, 95% CI = 0.70, 0.95, P = 0.01) as well as among smokers (OR = 0.74, 95% CI = 0.61, 0.90, P = 0.003). Yet, our data do not support the previously reported associations of HPGD tagSNPs and risk of CRC.

Journal Article.  3754 words. 

Subjects: Clinical Cytogenetics and Molecular Genetics

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