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Cancer Causes & Control
Erschienen in: Cancer Causes & Control 2/2008

01.03.2008 | Original Paper

Joint effect between regular use of non-steroidal anti-inflammatory drugs, variants in inflammatory genes and risk of lymphoma

verfasst von: Birgit Hoeft, Nikolaus Becker, Evelin Deeg, Lars Beckmann, Alexandra Nieters

Erschienen in: Cancer Causes & Control | Ausgabe 2/2008

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Abstract

Objective

Limited evidence suggests the importance of inflammatory processes for the etiology of lymphomas. To further research in this area, we investigated the role of genetic variants in key inflammatory factors, non-steroidal anti-inflammatory drug [NSAID] use, and their joint effect in lymphomagenesis.

Methods

The study comprised 710 case–control pairs, matched for gender, age, and study region. We examined the association of regular NSAID use and polymorphisms in prostaglandin-endoperoxide synthase-2 (COX2), prostaglandin E synthase (PTGES), interleukin-1 alpha (IL1A), IL-1 beta (IL1B), and IL-1 receptor antagonist (IL1RA), and lymphoma risk by applying logistic regression to calculate odds ratios (OR) and 95% confidence intervals (95% CI).

Results

Regular NSAID use was associated with a slightly reduced risk of B-NHL (OR = 0.8, 95% CI = 0.6–1.1). For T-NHL, the COX2 rs2745557 A-allele conferred a 2.2-fold (95% CI = 1.1–4.5) and homozygosis for the IL1RN rs454078 T-allele was associated with a 4.5-fold (95% CI = 1.4–13.9) elevated risk, however, based on sparse data. IL1 haplotype 5 was associated with a statistically significant 43% increased risk for B-NHL among non-regular users of NSAIDs, but a 70% decreased risk for regular users (p-value for interaction < 0.001).

Conclusions

These results suggest the relevance of joint effects between NSAID use and IL1 haplotypes on the risk of B-NHL.
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Metadaten
Titel
Joint effect between regular use of non-steroidal anti-inflammatory drugs, variants in inflammatory genes and risk of lymphoma
verfasst von
Birgit Hoeft
Nikolaus Becker
Evelin Deeg
Lars Beckmann
Alexandra Nieters
Publikationsdatum
01.03.2008
Verlag
Springer Netherlands
Erschienen in
Cancer Causes & Control / Ausgabe 2/2008
Print ISSN: 0957-5243
Elektronische ISSN: 1573-7225
DOI
https://doi.org/10.1007/s10552-007-9082-9

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