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Articles by J. A. Baron
Total Records ( 3 ) for J. A. Baron
  J. A. Baron
 

This perspective on Bertagnolli et al. (beginning on p. 588 in this issue of the journal) and Lipkin et al. (beginning on p. 597) considers the likelihood that statins have chemopreventive efficacy in the large bowel. An observational analysis within a clinical trial of celecoxib found no benefit of statin use on the risk of colorectal adenomas (and some suggestions of an adverse effect). On the other hand, variation in the 3-hydroxy-3-methylglutaryl coenzyme A reductase gene modified the association of statins with risk of colorectal cancer. The perspective discusses the implications of these data and how they fit into the context of previous investigations. Cancer Prev Res; 3(5); 573–5. ©2010 AACR.

  E. T Jacobs , M. E Martinez , P. T Campbell , D. V Conti , D Duggan , J. C Figueiredo , R. W Haile , E. C LeRoy , J. N Poynter , P. A Thompson and J. A. Baron
 

Genetic variants in the calcium/vitamin D metabolic pathway may be related to risk for colorectal cancer. While several investigations of vitamin D receptor (VDR) polymorphisms and colorectal cancer have been conducted, no studies to date have evaluated the association of genetic variation in the heterodimer partner for VDR, the retinoid X receptor (RXR). Another important gene in this pathway is the calcium-sensing receptor (CASR). Employing a discordant-sibship case–control design, we examined the association between single nucleotide polymorphisms (SNPs) in RXRA and CASR and risk for colorectal cancer overall and by colorectal subsite and microsatellite instability (MSI) status using data from the Colon Cancer Family Registry. No gene-level relationships between RXRA or CASR and colorectal cancer overall were observed. However, for RXRA SNP rs7861779, a high-interest SNP selected for study a priori, there was a statistically significantly increased risk for proximal colorectal cancer among those with at least one A allele [odds ratio (OR) = 1.42; 95% confidence interval (CI) = 1.03–1.97]. Another selected RXRA SNP, rs12004589, was significantly associated with risk of MSI-high cancers (OR = 2.27; 95% CI = 1.13–4.56). Additionally, CASR SNP rs1801726 was significantly associated with a reduced risk for rectal cancer (OR = 0.53; 95% CI = 0.29–0.96). These results provide support that RXRA SNPs rs7861779 and rs12004589 and CASR SNP rs1801726 may be important markers for colorectal neoplasia. Further work is needed to elucidate their role in the carcinogenic pathway.

  G. Y. F Ho , X Xue , M Cushman , G McKeown Eyssen , R. S Sandler , D. J Ahnen , E. L Barry , F Saibil , R. S Bresalier , T. E Rohan and J. A. Baron
 

The Aspirin/Folate Polyp Prevention Trial found that aspirin, but not folic acid, reduced recurrence of colorectal adenomas. This study examined whether treatment effects on inflammation markers explained the trial results. The trial had a factorial design with three aspirin (placebo, 81, and 325 mg/d) and two folic acid (placebo and 1 mg/d) groups. There were 884 subjects who had colonoscopic evaluation for adenomas at year 3 and plasma levels of C-reactive protein (CRP), interleukin 6 (IL-6), tumor necrosis factor (TNF-), soluble TNF receptor type II (sTNF-R2), and IL-1 receptor antagonist (IL-1Ra) measured at baseline and year 3. Among individuals not receiving folic acid, there was a 4% decrease (mean ratio of year 3 to baseline levels = 0.96, 95% confidence interval [CI] = 0.82 to 1.14) in CRP for a period of 3 years in the 325 mg of aspirin group vs a 20% increase (mean ratio = 1.20, 95% CI = 1.03 to 1.41) in the placebo group (P = .027). By contrast, the reverse was observed among individuals who also received folic acid (Pinteraction = .013). Changes in inflammation markers were not associated with adenoma recurrence. Low-dose aspirin (325 mg/d) is beneficial in stabilizing CRP levels, which may be abrogated by folate. Nevertheless, inflammation markers do not mediate the chemopreventive effect of aspirin on colorectal adenomas.

 
 
 
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