Minority Health and Health Equity Archive

Permanent URI for this collectionhttp://hdl.handle.net/1903/21769

Welcome to the Minority Health and Health Equity Archive (MHHEA), an electronic archive for digital resource materials in the fields of minority health and health disparities research and policy. It is offered as a no-charge resource to the public, academic scholars and health science researchers interested in the elimination of racial and ethnic health disparities.

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Author: search.filters.author.Henderson, Brian E.

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    Admixture mapping identifies 8q24 as a prostate cancer risk locus in African-American men
    (2006) Freedman, Matthew L.; Haiman, Christopher A.; Patterson, Nick; McDonald, Gavin J.; Tandon, Arti; Waliszewska, Alicja; Penney, Kathryn; Steen, Robert G.; Kristin Ardlie, Kristin; John, Esther M.; Oakley-Girvan, Ingrid; Whittemore, Alice S.; Cooney, Kathleen A.; Ingles, Sue A.; Altshuler, David; Henderson, Brian E.; Reich, David
    A whole-genome admixture scan in 1,597 African Americans identified a 3.8Mbinterval on chromosome 8q24 as significantly associated with susceptibility to prostate cancer [logarithm of odds (LOD)7.1]. The increased risk because of inheriting African ancestry is greater in men diagnosed before 72 years of age (P < 0.00032) and may contribute to the epidemiological observation that the higher risk for prostate cancer in African Americans is greatest in younger men (and attenuates with older age). The same region was recently identified through linkage analysis of prostate cancer, followed by fine-mapping. We strongly replicated this association (P<4.2109) but find that the previously described alleles do not explain more than a fraction of the admixture signal. Thus, admixture mapping indicates a major, still-unidentified risk gene for prostate cancer at 8q24, motivating intense work to find it.
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    Genome-wide association study identifies novel breast cancer susceptibility loci
    (2007) Easton, Douglas F.; Pooley, Karen A.; Dunning, Alison M.; Pharoah, Paul D. P.; Thompson, Deborah; Ballinger, Dennis G.; Struewing, Jeffery P.; Morrison, Jonathan; Field, Helen; Luben, Robert; Wareham, Nicholas; Ahmed, Shahana; Healey, Catherine S.; Bowman, Richard; Meyer, Kerstin B.; Haiman, Christopher A.; Kolonel, Laurence K.; Henderson, Brian E.; Le Marchand, Loic; Brennan, Paul; Sangrajrang, Suleeporn; Gaborieau, Valerie; Odefrey, Fabrice; Shen, Chen-Yang; Wu, Pei-Ei; Wang, Hui-Chun; Eccles, Diana; Evans, D. Gareth; Peto, Julian; Fletcher, Olivia; Johnson, Nichola; Seal, Sheila; Stratton, Michael R.; Rahman, Nazneen; Chenevix-Trench, Georgia; Bojesen, Stig E.; Nordestgaard, Børge G.; Axelsson, Christen K.; Garcia-Closas, Montserrat; Brinton, Louise; Chanock, Stephen; Lissowska, Jolanta; Peplonska, Beata; Nevanlinna, Heli; Fagerholm, Rainer; Eerola, Hannaleena; Kang, Daehee; Yoo, Keun-Young; Noh, Dong-Young; Ahn, Sei-Hyun; Hunter, David J.; Hankinson, Susan E.; Cox, David G.; Hall, Per; Wedren, Sara; Liu, Jianjun; Low, Yen-Ling; Bogdanova, Natalia; Schu¨rmann, Peter; Do¨rk, Do¨rk; Tollenaar, Rob A. E. M.; Jacobi, Catharina E.; Devilee, Peter; Klijn, Jan G. M.; Sigurdson, Alice J.; Doody, Michele M.; Alexander, Bruce H.; Zhang, Jinghui; Cox, Angela; Brock, Ian W.; MacPherson, Gordon; Reed, Malcolm W. R.; Couch, Fergus J.; Goode, Ellen L.; Olson, Janet E.; Meijers-Heijboer, Hanne; van den Ouweland, Ans; Uitterlinden, Andre´; Rivadeneira, Fernando; Milne, Roger L.; Ribas, Gloria; Gonzalez-Neira, Anna; Benitez, Javier; Hopper, John L.; McCredie, Margaret; Southey, Melissa; Giles, Graham G.; Schroen, Chris; Justenhoven, Christina; Brauch, Hiltrud; Hamann, Ute; Ko, Yon-Dschun; Spurdle, Amanda B.; Beesley, Jonathan; Chen, Xiaoqing; kConFab, _; the SEARCH, collaborators; AOCS, Management Group; Mannermaa, Arto; Kosma, Veli-Matti; Kataja, Vesa; Hartikainen, Jaana; Day, Nicholas E.; Cox, David R.; Ponder, Bruce A. J.
    Breast cancer exhibits familial aggregation, consistent with variation in genetic susceptibility to the disease. Known susceptibility genes account for less than 25% of the familial risk of breast cancer, and the residual genetic variance is likely to be due to variants conferring more moderate risks. To identify further susceptibility alleles, we conducted a two-stage genome-wide association study in 4,398 breast cancer cases and 4,316 controls, followed by a third stage in which 30 single nucleotide polymorphisms (SNPs) were tested for confirmation in 21,860 cases and 22,578 controls from 22 studies. We used 227,876 SNPs that were estimated to correlate with 77% of known common SNPs in Europeans at r2.0.5. SNPs in five novel independent loci exhibited strong and consistent evidence of association with breast cancer (P,1027). Four of these contain plausible causative genes (FGFR2, TNRC9, MAP3K1 and LSP1). At the second stage, 1,792 SNPs were significant at the P,0.05 level compared with an estimated 1,343 that would be expected by chance, indicating that many additional common susceptibility alleles may be identifiable by this approach.
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    Systematic Evaluation of Genetic Variation at the Androgen Receptor Locus and Risk of Prostate Cancer in a Multiethnic Cohort Study
    (2005) Freedman, Matthew L.; Pearce, Celeste L.; Penney, Kathryn L.; Hirschhorn, Joel N.; Kolonel, Laurence N.; Henderson, Brian E.; Altshuler, David
    Repeat length of the CAG microsatellite polymorphism in exon 1 of the androgen receptor (AR) gene has been associated with risk of prostate cancer in humans. This association has been the focus of >20 primary epidemiological publications and multiple review articles, but a consistent and reproducible association has yet to be confirmed. We systematically addressed possible causes of false-negative and false-positive association in >4,000 individuals from a multiethnic, prospective cohort study of prostate cancer, comprehensively studying genetic variation by microsatellite genotyping, direct resequencing of exons in advanced cancer cases, and haplotype analysis across the 180-kb AR genomic locus. These data failed to confirm that common genetic variation in the AR gene locus influences risk of prostate cancer. A systematic approach that assesses both coding and noncoding genetic variation in large and diverse patient samples can help clarify hypotheses about association between genetic variants and disease.
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    Physical Exercise and Reduced Risk of Breast Cancer in Young Women
    (1994) Bernstein, Leslie; Henderson, Brian E.; Hanisch, Rosemarie; Sullivan-Halley, Jane; Ross, Ronald K.
    Background: Epidemiologic evidence strongly suggests that cumulative exposure to ovarian hormones is a determinant of breast cancer risk. Because physical activity can modify menstrual cycle patterns and alter the production of ovarian hormones, it may reduce breast cancer risk; yet few epidemiologic studies have assessed this relationship. Purpose: The major objective of this study was to determine whether young women (aged 40 and younger) who regularly participated in physical exercise activities during their reproductive years had a reduced risk of breast cancer. Methods: Using a case-control design, we conducted personal interviews of a total of 545 women (aged 40 and younger at diagnosis) who had been newly diagnosed with in situ or invasive breast cancer between July 1, 1983, and January 1, 1989, and a total of 545 control subjects. Case patients and control subjects were individually matched on date of birth (within 36 months), race (white), parity (nulliparous versus parous), and neighborhood of residence. Lifetime histories of participation in physical exercise activities on a regular basis were obtained during the personal interview. Results: After adjustment for potential confounding factors, we found that the average number of hours spent in physical exercise activities per week from menarche to 1 year prior to the case patient's diagnosis was a significant predictor of reduced breast cancer risk (two-sided P for trend < .0001). The odds ratio (OR) of breast cancer among women who, on average, spent 3.8 or more hours per week participating in physical exercise activities was 0.42 (95% confidence limits [CLs] = 0.27, 0.64) relative to inactive women. The effect was stronger among women who had had a full-term pregnancy. Comparing most active (>/= 3.8 hours/wk of exercise) women to inactive women, the ORs were 0.28 (95% CL = 0.16, 0.50) for parous and 0.73 (95% CL = 0.38, 1.41) for nulliparous women. Conclusions: Most previously identified risk factors for breast cancer are reproductive and menstrual events that cannot be readily altered. The protective effect of exercise on breast cancer risk in the women whom we studied suggests that physical activity offers one modifiable lifestyle characteristic that may substantially reduce a woman's lifetime risk of breast cancer. Implications: Whether the protective effects of exercise on breast cancer risk are due to alterations in ovarian function and whether they extend into women's menopausal years need to be established. Our results suggest that implementation of regular physical exercise programs as a critical component of a healthy lifestyle should be a high priority for adolescent and adult women.
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    Ethnic and Racial Differences in the Smoking-Related Risk of Lung Cancer
    (2006) Haiman, Christopher A.; Stram, Daniel O.; Wilkens, Lynne R.; Pike, Malcolm C.; Kolonel, Laurence N.; Henderson, Brian E.; Le Marchand, Loïc
    Background There is remarkable variation in the incidence of lung cancer among ethnic and racial groups in the United States. Methods We investigated differences in the risk of lung cancer associated with cigarette smoking among 183,813 African-American, Japanese-American, Latino, Native Hawaiian, and white men and women in the Multiethnic Cohort Study. Our analysis included 1979 cases of incident lung cancer identified prospectively over an eight-year period, between baseline (1993 through 1996) and 2001. Results The risk of lung cancer among ethnic and racial groups was modified by the number of cigarettes smoked per day. Among participants who smoked no more than 30 cigarettes per day, African Americans and Native Hawaiians had significantly greater risks of lung cancer than did the other groups. Among those who smoked no more than 10 and those who smoked 11 to 20 cigarettes per day, relative risks ranged from 0.21 to 0.39 (P<0.001) among Japanese Americans and Latinos and from 0.45 to 0.57 (P<0.001) among whites, as compared with African Americans. However, at levels exceeding 30 cigarettes per day, these differences were not significant. Differences in risk associated with smoking were observed among both men and women and for all histologic types of lung cancer. Conclusions Among cigarette smokers, African Americans and Native Hawaiians are more susceptible to lung cancer than whites, Japanese Americans, and Latinos.