Journal of the National Cancer Institute Advance Access originally published online on March 11, 2008
JNCI Journal of the National Cancer Institute 2008 100(6):444-445; doi:10.1093/jnci/djn017
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© The Author 2008. Published by Oxford University Press.
CORRESPONDENCE |
Response: Re: C-Reactive Protein and Risk of Breast Cancer
Affiliations of authors: Division of Preventive Medicine (SMZ, PMR), Center for Cardiovascular Disease Prevention (PMR), and Donald W. Reynolds Center for Cardiovascular Research (PMR), Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA; Department of Epidemiology, Harvard School of Public Health, Boston, MA (PMR)
Correspondence to: Shumin M. Zhang, MD, ScD, Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital, 900 Commonwealth Ave East, Boston, MA 02215 (e-mail: shumin.zhang{at}channing.harvard.edu).
We thank Zeleniuch-Jacquotte et al. for their interest in our paper, which showed no statistically significant positive association between baseline plasma C-reactive protein (CRP) levels and breast cancer risk in a prospective analysis involving 892 case patients among 27919 women followed-up for an average of 10 years in the Women's Health Study. They reported a statistically significant positive association between baseline CRP and breast cancer risk in a nested case–control analysis of 85 postmenopausal women who were diagnosed with breast cancer between 6 months and 5.5 years following blood collection and 163 matched control subjects in the New York University Women's Health Study. In an analysis of the Women's Health Study data restricted to the first 5 years of follow-up, we continued to find no statistically significant positive association between baseline CRP and breast cancer risk among either premenopausal or postmenopausal women. In fact, among postmenopausal women, a statistically significant inverse association between baseline CRP and breast cancer risk was observed instead (Table 1).
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The median CRP value (range = 0.29–0.72 mg/L) in the New York University Women's Health Study was much lower than that in the Women's Health Study (2.0 mg/L) and other cohorts of postmenopausal women (1,2). Moreover, CRP tertiles were categorized according to the distribution in both case patients and control subjects rather than in control subjects only and thus may not represent the distribution in the source population that generated the case patients. Nevertheless, in the New York University Women's Health Study, statistically significant positive associations between baseline CRP and risk of breast cancer were observed for both categorical and continuous classifications of CRP among postmenopausal women, and such positive associations were attenuated after controlling for body mass index (BMI). In the Women's Health Study, CRP levels were also positively correlated with BMI (Spearman r = .47 for all women; r = .55 for premenopausal women; r = .42 for postmenopausal women), but additional adjustment for BMI in models adjusted for age and randomized treatment assignment did not appreciably change the hazard ratios among postmenopausal women (Table 1). The associations between baseline CRP and breast cancer risk differed according to categories of BMI among postmenopausal women (Pinteraction = .04 for first 5 years of follow-up; Pinteraction = .06 for the full length of follow-up); there was a statistically significant inverse association between baseline CRP and breast cancer risk in women with BMI of 25 kg/m2 or greater (Ptrend = .004 and Ptrend = .04 for first 5 years and the full length of follow-up, respectively) but no statistically significant positive association in women with BMI less than 25 kg/m2 (Ptrend = .59 and Ptrend = .81 for first 5 years and the full length of follow-up, respectively). There were no statistically significant associations between baseline CRP and breast cancer risk by categories of BMI among premenopausal women (Pinteraction = .32 for first 5 years of follow-up; Pinteraction = .24 for the full length of follow-up). These data suggest that the lack of statistically significant positive associations in the Women's Health Study is unlikely to be explained by BMI and menopausal status.
REFERENCES
1. Liu S, Tinker L, Song Y, et al. A prospective study of inflammatory cytokines and diabetes mellitus in a multiethnic cohort of postmenopausal women. Arch Intern Med (2007) 167(15):1676–1685.
2. Pai JK, Pischon T, Ma J, et al. Inflammatory markers and the risk of coronary heart disease in men and women. N Engl J Med (2004) 351(25):2599–2610.
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J Natl Cancer Inst 2008 100: 443-444.
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