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- Feigelson, HS, et al.
(författare)
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Haplotype analysis of the HSD17B1 gene and risk of breast cancer: A comprehensive approach to multicenter analyses of prospective cohort studies
- 2006
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Ingår i: Cancer Research. - 1538-7445. ; 66:4, s. 2468-2475
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Tidskriftsartikel (refereegranskat)abstract
- The 17 beta-hydroxysteroid dehydrogenase 1 gene (HSD17B1) encodes 17HSD1, which catalyzes the final step of estradiol biosynthesis. Despite the important role of HSD17B1 in hormone metabolism, few epidemiologic studies of HSD17B1 and breast cancer have been conducted. This study includes 5,370 breast cancer cases and 7,480 matched controls from five large cohorts in the Breast and Prostate Cancer Cohort Consortium. We characterized variation in HSD17B1 by resequencing and dense genotyping a multiethnic sample and identified haplotype-tagging single nucleotide polymorphisms (htSNP) that capture common variation within a 33.3-kb region around HSD17B1. Four htSNPs, including the previously studied SNP rs605059 (S312G), were genotyped to tag five common haplotypes in all cases and controls. Conditional logistic regression was used to estimate odds ratios (OR) for disease. We found no evidence of association between common HSD17B1 haplotypes or htSNPs and overall risk of breast cancer. The OR for each haplotype relative to the most common haplotype ranged from 0.98 to 1.07 (omnibus test for association: X-2 = 3.77, P = 0.58, 5 degrees of freedom). When cases were subdivided by estrogen receptor (ER) status, two common haplotypes were associated with ER-negative tumors (test for trend, Ps = 0.0009 and 0.0076; n = 353 cases). HSD17B1 variants that are common in Caucasians are not associated with overall risk of breast cancer; however, there was an association among the subset of ER-negative tumors. Although the probability that these ER-negative findings are false-positive results is high, these findings were consistent across each cohort examined and warrant further study.
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| 3. |
- Bauer, D. C., et al.
(författare)
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Classification of osteoarthritis biomarkers: a proposed approach
- 2006
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Ingår i: Osteoarthritis and Cartilage. - : Elsevier BV. - 1063-4584. ; 14:8, s. 723-727
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Forskningsöversikt (refereegranskat)abstract
- Objective: Osteoarthritis (OA) biomarkers are needed by researchers and clinicians to assist in disease diagnosis and assessment of disease severity, risk of onset, and progression. As effective agents for CA are developed and tested in clinical studies, biomarkers; that reliably mirror or predict the progression or amelioration of CA will also be needed. Methods: The NIH-funded CA Biomarkers Network is a multidisciplinary group interested in the development and validation of CA biomarkers. This review summarizes our efforts to characterize and classify CA biomarkers. Results: We propose the "BIPED" biomarker classification (which stands for Burden of Disease, Investigative, Prognostic, Efficacy of Intervention and Diagnostic), and offer suggestions on optimal study design and analytic methods for use in CA investigations. Conclusion. The BIPED classification provides specific biomarker definitions with the goal of improving our ability to develop and analyze OA biomarkers, and to communicate these advances within a common framework. (C) 2006 OsteoArthritis Research Society International. Published by Elsevier Ltd. All rights reserved.
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| 5. |
- Genkinger, J M, et al.
(författare)
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Dairy products and ovarian cancer : A pooled analysis of 12 cohort studies
- 2006
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Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA. Brigham & Womens Hosp, Channing Lab, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA. Brigham & Womens Hosp, Div Prevent Med, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA USA. Univ Minnesota, Sch Publ Hlth, Div Epidemiol, Minneapolis, MN 55455 USA. NYU, Dept Environm Med, Div Epidemiol, New York, NY 10016 USA. Loma Linda Univ, Sch Med, Ctr Hlth Res, Loma Linda, CA USA. SUNY Buffalo, Dept Social & Prevent Med, Buffalo, NY 14260 USA. Netherlands Org Appl Sci Res Qual Life, Dept Food & Chem Risk Anal, Zeist, Netherlands. Univ Oslo, Dept Nutr, Oslo, Norway. NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. Natl Inst Environm Med, Div Nutr Epidemiol, Karolinska Inst, Stockholm, Sweden. Amer Canc Soc, Atlanta, GA 30329 USA. Univ Toronto, Fac Med, Dept Publ Hlth Sci, Toronto, ON, Canada. Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10467 USA. Maastricht Univ, Dept Epidemiol, Nutr & Toxicol Res Inst, Maastricht, Netherlands. : AMER ASSOC CANCER RESEARCH. - 1055-9965 .- 1538-7755. ; 15:2, s. 364-372
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Tidskriftsartikel (refereegranskat)abstract
- Background: Dairy foods and their constituents (lactose and calcium) have been hypothesized to promote ovarian carcinogenesis. Although case-control studies have reported conflicting results for dairy foods and lactose, several cohort studies have shown positive associations between skim milk, lactose, and ovarian cancer. Methods: A pooled analysis of the primary data from 12 prospective cohort studies was conducted. The study population consisted of 553,217 women among whom 2,132 epithelial ovarian cases were identified. Study-specific relative risks and 95% confidence intervals were calculated by Cox proportional hazards models and then pooled by a random-effects model. Results: No statistically significant associations were observed between intakes of milk, cheese, yogurt, ice cream, and dietary and total calcium intake and risk of ovarian cancer. Higher lactose intakes comparing >= 30 versus < 10 g/d were associated with a statistically significant higher risk of ovarian cancer, although the trend was not statistically significant (pooled multivariate relative risk, 1.19; 95% confidence interval, 1.01-1.40; P-trend = 0.19). Associations for endometrioid, mucinous, and serous ovarian cancer were similar to the overall findings. Discussion: Overall, no associations were observed for intakes of specific dairy foods or calcium and ovarian cancer risk. A modest elevation in the risk of ovarian cancer was seen for lactose intake at the level that was equivalent to three or more servings of milk per day. Because a new dietary guideline recommends two to three servings of dairy products per day, the relation between dairy product consumption and ovarian cancer risk at these consumption levels deserves further examination.
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| 9. |
- Englund, Martin, et al.
(författare)
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Effect of meniscal damage on the development of frequent knee pain, aching, or stiffness
- 2007
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Ingår i: Arthritis and Rheumatism. - : Wiley. - 1529-0131 .- 0004-3591. ; 56:12, s. 4048-4054
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: To evaluate the effect of meniscal damage on the development of frequent knee pain, aching, or stiffness in middle-aged and older adults. METHODS: The Multicenter Osteoarthritis Study is a prospective study of 3,026 individuals 50 years of age or older who have or are at high risk of developing knee osteoarthritis (OA). We investigated knees at baseline and at 15 months. Case knees (n = 110) were those with no pain, aching, or stiffness on most days at baseline, but that had developed frequent pain, aching, or stiffness at 15 months. Control knees (n = 220) were drawn randomly from knees with no frequent symptoms at baseline that did not become case knees. Using 1.0T magnetic resonance imaging performed at baseline and at followup, 2 musculoskeletal radiologists blinded to the case-control status assessed the meniscal damage using the following scale: 0 = intact, 1 = minor tear, 2 = nondisplaced tear or prior surgical repair, and 3 = displaced tear, resection, maceration, or destruction. The effect of meniscal damage was analyzed by contingency tables and logistic regression. RESULTS: Meniscal damage was common at baseline both in case knees (38%) and in control knees (29%). Although there was a modest association between the meniscal damage score (range 0-3) and the development of frequent knee pain, aching, or stiffness (odds ratio [OR] 1.21, 95% confidence interval [95% CI] 0.96-1.51, adjusted for age, sex, and body mass index), meniscal damage was mostly present in knees with OA. When considering the co-occurrence of OA, we found no independent association between meniscal damage and the development of frequent knee symptoms (OR 1.05, 95% CI 0.80-1.37). CONCLUSION: In middle-aged and older adults, any association between meniscal damage and the development of frequent knee pain seems to be present because both pain and meniscal damage are related to OA and not because of a direct link between the two.
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| 10. |
- Genkinger, J M, et al.
(författare)
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A pooled analysis of 12 cohort studies of dietary fat, cholesterol and egg intake and ovarian cancer
- 2006
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Ingår i: Cancer Causes and Control. - Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA. Harvard Univ, Sch Med, Boston, MA USA. Harvard Univ, Sch Publ Hlth, Harvard Ctr Canc Prevent, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA. Univ Minnesota, Sch Publ Hlth, Div Epidemiol, Minneapolis, MN 55455 USA. Loma Linda Univ, Sch Med, Ctr Hlth Res, Loma Linda, CA USA. Brigham & Womens Hosp, Div Prevent Med, Boston, MA 02115 USA. SUNY Buffalo, Dept Social & Prevent Med, Buffalo, NY 14260 USA. : SPRINGER. - 0957-5243 .- 1573-7225. ; 17:3, s. 273-285
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Tidskriftsartikel (refereegranskat)abstract
- Fat and cholesterol are theorized to promote ovarian carcinogenesis by increasing circulating estrogen levels. Although case-control studies have reported positive associations between total and saturated fat intake and ovarian cancer risk, two cohort studies have observed null associations. Dietary cholesterol and eggs have been positively associated with ovarian cancer risk. A pooled analysis was conducted on 12 cohort studies. Among 523,217 women, 2,132 incident epithelial ovarian cancer cases were identified. Study-specific relative risks (RR) and 95% confidence intervals (CI) were calculated by Cox proportional hazards models, and then pooled using a random effects model. Total fat intake was not associated with ovarian cancer risk (pooled multivariate RR = 1.08, 95% CI 0.86-1.34 comparing >= 45 to 30-< 35% of calories). No association was observed for monounsaturated, polyunsaturated, trans-unsaturated, animal and vegetable fat, cholesterol and egg intakes with ovarian cancer risk. A weakly positive, but non-linear association, was observed for saturated fat intake (pooled multivariate RR = 1.29, 95% CI: 1.01-1.66 comparing highest versus lowest decile). Results for histologic subtypes were similar. Overall, fat, cholesterol and egg intakes were not associated with ovarian cancer risk. The positive association for saturated fat intake at very high intakes merits further investigation.
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