ArticlePharmacogenetics and genomics2009
C-reactive protein genotypes and haplotypes, polymorphisms in NSAID-metabolizing enzymes, and risk of colorectal polyps.
Article in Pharmacogenetics and genomics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- C-reactive protein and risk of colorectal adenomas or serrated polyps: a prospective study.Cancer prevention research (Philadelphia, Pa.) · 2014Trial
- Polymorphisms in genes related to inflammation and obesity and colorectal adenoma risk.Molecular carcinogenesis · 2018Article
- Prognostic significance of C-reactive protein polymorphism and KRAS/BRAF in synchronous liver metastasis from colorectal cancer.PloS one · 2014Article
- Genetic variation in C-reactive protein in relation to colon and rectal cancer risk and survival.International journal of cancer · 2011Article
- Cyclooxygenase-2 and cancer treatment: understanding the risk should be worth the reward.Clinical cancer research : an official journal of the American Association for Cancer Research · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
Abstract
introductionC-reactive protein (CRP) is a nonspecific marker of inflammation linked to cardiovascular disease and possibly colon cancer. Polymorphisms in CRP have been associated with differential CRP concentrations among healthy adults, with some evidence for functional effects on CRP expression.
methodsA linkage disequilibrium-based tag single nucleotide polymorphism (SNP)-selection algorithm identified six tagSNPs for Europeans (-821A>G, -390C>T/A, 90A>T, 838G>C, 2043G>A, and 4363C>A), defining six haplotypes with more than 1% frequency. In a case-control study of adenomatous (n=491) or hyperplastic (n=184) polyps versus polyp-free controls (n=583) we investigated these SNPs in relation to colorectal polyp risk.
resultsIndividuals with 838 GC or CC genotypes had a modestly, although not statistically significantly, increased risk of adenomas (odds ratio: 1.4 95% confidence interval: 0.9-2.1) and a nearly 2-fold increased risk of concurrent adenomas and hyperplastic polyps (odds ratio: 2.0 95% confidence interval: 1.1-3.6). Increased risk for concurrent adenomas and hyperplastic polyps was also observed for haplotype ACACAC. No other main associations were detected. Risk of adenomas associated with 2043G>A differed with nonsteroidal anti-inflammatory drug (NSAID) use. Among NSAID nonusers, there was a suggestion that the GA or AA genotypes were associated with decreased risk of adenomas; this was not seen among NSAID users (P interaction=0.03). We also observed interactions between UGT1A1 [TA](7) promoter repeat polymorphism and CRP tagSNPs -390C>T/A and 90A>T, in which only the homozygous variant CRP genotype was associated with increased risk of adenoma among those with the UGT1A1 6rpt/6rpt genotype (P interaction=0.02 and 0.04 for -390C>T/A and 90A>T, respectively).
conclusionThese results provide limited support for associations between genetic variation in CRP and colorectal polyp risk. The observed interactions should be evaluated further.
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