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  • 1
    Keywords: CANCER ; neoplasms ; POLYMORPHISMS ; UNITED-STATES ; ALCOHOL-CONSUMPTION ; SAN-FRANCISCO ; AGGREGATION ; FRANCISCO BAY AREA ; CONNECTICUT WOMEN ; MIGRANTS
    Abstract: A role for genetic susceptibility in non-Hodgkin lymphoma (NHL) is supported by the accumulating evidence of common genetic variations altering NHL risk. However, the pattern of NHL heritability remains poorly understood. We conducted a pooled analysis of 10 211 NHL cases and 11905 controls from the International Lymphoma Epidemiology Consortium (InterLymph) to evaluate NHL risk among those with hematopoietic malignancies in first-degree relatives. Odds ratios (ORs) and 95% confidence intervals (CIs) of NHL and its subtypes were estimated from unconditional logistic regression models with adjustment for confounders. NHL risk was elevated for individuals who reported first-degree relatives with NHL (OR = 1.5; 95% CI = 1.2-1.9), Hodgkin lymphoma (OR = 1.6; 95% Cl = 1.1-2.3), and leukemia (OR = 1.4; 95% CI = 1.2-2.7). Risk was highest among individuals who reported a brother with NHL (OR = 2.8; 95% CI = 1.6-4.8) and was consistent for all NHL subtypes evaluated. If a first-degree relative had Hodgkin lymphoma, NHL risk was highest if the relative was a parent (OR = 1.7; 95% CI = 1.0-2.9). If a first-degree relative had leukemia, NHL risk was highest among women who reported a sister with leukemia (OR = 3.0; 95% CI = 1.6-5.6). The pattern of NHL heritability appeared to be uniform across NHL subtypes, but risk patterns differed by specific hematopoietic malignancies and the sex of the relative, revealing critical clues to disease etiology.
    Type of Publication: Journal article published
    PubMed ID: 17185468
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  • 2
    Keywords: CANCER ; THERAPY ; INFORMATION ; COHORT ; DISEASE ; incidence ; RISK ; RISK-FACTORS ; BREAST ; BREAST-CANCER ; DESIGN ; AGE ; WOMEN ; PROSPECTIVE COHORT ; smoking ; cancer risk ; UNITED-STATES ; ALCOHOL ; ALCOHOL-CONSUMPTION ; CONSUMPTION ; BIRTH COHORT ; POSTMENOPAUSAL WOMEN ; MASS INDEX ; ORAL-CONTRACEPTIVE USE ; REQUIRING PROLONGED OBSERVATION ; METAANALYSIS ; HORMONAL FACTORS ; ANTHROPOMETRIC MEASURES ; EPITHELIAL OVARIAN
    Abstract: BACKGROUND: Only about half the studies that have collected information on the relevance of women's height and body mass index to their risk of developing ovarian cancer have published their results, and findings are inconsistent. Here, we bring together the worldwide evidence, published and unpublished, and describe these relationships. METHODS AND FINDINGS: Individual data on 25,157 women with ovarian cancer and 81,311 women without ovarian cancer from 47 epidemiological studies were collected, checked, and analysed centrally. Adjusted relative risks of ovarian cancer were calculated, by height and by body mass index. Ovarian cancer risk increased significantly with height and with body mass index, except in studies using hospital controls. For other study designs, the relative risk of ovarian cancer per 5 cm increase in height was 1.07 (95% confidence interval [CI], 1.05-1.09; p〈0.001); this relationship did not vary significantly by women's age, year of birth, education, age at menarche, parity, menopausal status, smoking, alcohol consumption, having had a hysterectomy, having first degree relatives with ovarian or breast cancer, use of oral contraceptives, or use of menopausal hormone therapy. For body mass index, there was significant heterogeneity (p〈0.001) in the findings between ever-users and never-users of menopausal hormone therapy, but not by the 11 other factors listed above. The relative risk for ovarian cancer per 5 kg/m(2) increase in body mass index was 1.10 (95% CI, 1.07-1.13; p〈0.001) in never-users and 0.95 (95% CI, 0.92-0.99; p = 0.02) in ever-users of hormone therapy. CONCLUSIONS: Ovarian cancer is associated with height and, among never-users of hormone therapy, with body mass index. In high-income countries, both height and body mass index have been increasing in birth cohorts now developing the disease. If all other relevant factors had remained constant, then these increases in height and weight would be associated with a 3% increase in ovarian cancer incidence per decade. Please see later in the article for the Editors' Summary.
    Type of Publication: Journal article published
    PubMed ID: 22606070
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  • 3
    Keywords: CANCER ; MODEL ; SUPPORT ; EPIDEMIOLOGY ; LONG-TERM ; RISK ; COMPONENTS ; ASSOCIATION ; NO ; LYMPHOMA ; WOMEN ; MEN ; OBESITY ; UNITED-STATES ; case-control studies ; ALCOHOL-CONSUMPTION ; nutrition ; B-CELL LYMPHOMA ; ONCOLOGY ; case-control study ; REGRESSION ; MALIGNANT-LYMPHOMA ; WEIGHT ; PHYSICAL-ACTIVITY ; HEIGHT ; non-Hodgkin lymphoma ; analysis ; diffuse large B-cell lymphoma ; SUBTYPES ; BODY-MASS INDEX ; pooled analysis ; OVERWEIGHT ; USA ; BMI ; RISK-FACTOR ; CANCER-RISK ; B-CELL ; ENGLAND ; RATIO ; non Hodgkin lymphoma ; EXCESS ; POOLED-ANALYSIS ; NO EVIDENCE ; non-Hodgkin ; CONSORTIUM ; nutritional status ; INTERLYMPH ; body mass index weight ; FORMER COLLEGE-STUDENTS ; LYMPHOHEMATOPOIETIC MALIGNANCIES ; SCANDINAVIAN MEN
    Abstract: Nutritional status is known to alter immune function, a suspected risk factor for non-Hodgkin lymphoma (NHL). To investigate whether long-term over, or under, nutrition is associated with NHL, self-reported anthropometric data on weight and height from over 10,000 cases of NHL and 16,000 controls were pooled across 18 case-control studies identified through the International Lymphoma Epidemiology Consortium. Study-specific odds ratios (OR) were estimated using logistic regression and combined using a random-effects model. Severe obesity, defined as BMI of 40 kg m(-2) or more, was not associated with NHL overall (pooled OR = 1.00, 95% confidence interval (CI) 0.70-1.41) or the majority of NHL subtypes. An excess was however observed for diffuse large B-cell lymphoma (pooled OR = 1.80, 95% CI 1.24-2.62), although not all study-specific ORs were raised. Among the overweight (BMI 25-29.9 kg m(-2)) and obese (BMI 30-39.9 kg m(-2)), associations were elevated in some studies and decreased in others, while no association was observed among the underweight (BMI 〈 18.5 kg m(-2)). There was little suggestion of increasing ORs for NHL or its subtypes with every 5 kg m(-2) rise in BMI above 18.5 kg m(-2). BMI components height and weight were also examined, and the tallest men, but not women, were at marginally increased risk (pooled OR = 1.19, 95% CI 1.06-1.34). In summary, whilst we conclude that there is no evidence to support the hypothesis that obesity is a determinant of all types of NHL combined, the association between severe obesity and diffuse large B-cell lymphoma may warrant further investigation. (C) 2007 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 18167059
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