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Articles by D. R Bickers
Total Records ( 3 ) for D. R Bickers
  J. Y Tang , A Wu , E Linos , N Parimi , W Lee , M Aszterbaum , M. M Asgari , D. R Bickers and E. H. Epstein
 

Objectives  To evaluate vitamin D status in patients with basal cell nevus syndrome (BCNS) who practice photoprotection because of their genetic predisposition to skin cancer and to determine risk factors for deficiency.

Design  Retrospective cohort study.

Setting  Academic medical centers.

Patients  Forty-one ambulatory patients with BCNS who participated in a 2-year chemoprevention clinical trial. Population-based controls (n = 360) were selected and matched by age, sex, Fitzpatrick skin type, and season/geography.

Main Outcome Measures  Levels of 25-hydroxyvitamin D (25[OH]D) and vitamin D deficiency (defined as a 25[OH]D level of ≤20 ng/mL).

Results  Twenty-three patients with BCNS (56%) were vitamin D deficient. Patients with BCNS had mean 25(OH)D levels below those of the general population (–3 ng/mL; P = .02) and were 3 times more likely to be vitamin D deficient (56% vs 18%; P < .001). Levels of 25(OH)D were lower in patients who were overweight (–3.0 ng/mL; P = .04) and who had blood collected in the winter compared with the summer (–7.1 ng/mL; P < .001).

Conclusion  Patients with BCNS may be at increased risk for vitamin D deficiency, depending on their adherence to photoprotection practices.

Trial Registration  clinicaltrials.gov Identifier: NCT00023621

  J. Y Tang , M Aszterbaum , M Athar , F Barsanti , C Cappola , N Estevez , J Hebert , J Hwang , Y Khaimskiy , A Kim , Y Lu , P. L So , X Tang , M. A Kohn , C. E McCulloch , L Kopelovich , D. R Bickers and E. H. Epstein
 

In vitro and epidemiologic studies favor the efficacy of nonsteroidal anti-inflammatory drugs (NSAID) in preventing skin squamous photocarcinogenesis, but there has been relatively little study of their efficacy in preventing the more common skin basal cell carcinoma (BCC) carcinogenesis. We first compared the relative anti-BCC effects of genetic deletion and NSAID pharmacologic inhibition of cyclooxygenase (COX) enzymes in the skin of Ptch1+/– mice. We then assessed the effects of celecoxib on the development of BCCs in a 3-year, double-blinded, randomized clinical trial in 60 (PTCH1+/–) patients with the basal cell nevus syndrome. In Ptch1+/– mice, genetic deletion of COX1 or COX2 robustly decreased (75%; P < 0.05) microscopic BCC tumor burden, but pharmacologic inhibition with celecoxib reduced microscopic BCCs less efficaciously (35%; P < 0.05). In the human trial, we detected a trend for oral celecoxib reducing BCC burden in all subjects (P = 0.069). Considering only the 60% of patients with less severe disease (<15 BCCs at study entry), celecoxib significantly reduced BCC number and burden: subjects receiving placebo had a 50% increase in BCC burden per year, whereas subjects in the celecoxib group had a 20% increase (Pdifference = 0.024). Oral celecoxib treatment inhibited BCC carcinogenesis in PTCH1+/– mice and had a significant anti-BCC effect in humans with less severe disease. Cancer Prev Res; 3(1); OF1–11

 
 
 
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