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52. Imputation and subset-based association analysis across different cancer types identifies multiple independent risk loci in the TERT-CLPTM1L region on chromosome 5p15.33

Author

Wang, Z., primary, Zhu, B., additional, Zhang, M., additional, Parikh, H., additional, Jia, J., additional, Chung, C. C., additional, Sampson, J. N., additional, Hoskins, J. W., additional, Hutchinson, A., additional, Burdette, L., additional, Ibrahim, A., additional, Hautman, C., additional, Raj, P. S., additional, Abnet, C. C., additional, Adjei, A. A., additional, Ahlbom, A., additional, Albanes, D., additional, Allen, N. E., additional, Ambrosone, C. B., additional, Aldrich, M., additional, Amiano, P., additional, Amos, C., additional, Andersson, U., additional, Andriole, G., additional, Andrulis, I. L., additional, Arici, C., additional, Arslan, A. A., additional, Austin, M. A., additional, Baris, D., additional, Barkauskas, D. A., additional, Bassig, B. A., additional, Beane Freeman, L. E., additional, Berg, C. D., additional, Berndt, S. I., additional, Bertazzi, P. A., additional, Biritwum, R. B., additional, Black, A., additional, Blot, W., additional, Boeing, H., additional, Boffetta, P., additional, Bolton, K., additional, Boutron-Ruault, M.-C., additional, Bracci, P. M., additional, Brennan, P., additional, Brinton, L. A., additional, Brotzman, M., additional, Bueno-de-Mesquita, H. B., additional, Buring, J. E., additional, Butler, M. A., additional, Cai, Q., additional, Cancel-Tassin, G., additional, Canzian, F., additional, Cao, G., additional, Caporaso, N. E., additional, Carrato, A., additional, Carreon, T., additional, Carta, A., additional, Chang, G.-C., additional, Chang, I.-S., additional, Chang-Claude, J., additional, Che, X., additional, Chen, C.-J., additional, Chen, C.-Y., additional, Chen, C.-H., additional, Chen, C., additional, Chen, K.-Y., additional, Chen, Y.-M., additional, Chokkalingam, A. P., additional, Chu, L. W., additional, Clavel-Chapelon, F., additional, Colditz, G. A., additional, Colt, J. S., additional, Conti, D., additional, Cook, M. B., additional, Cortessis, V. K., additional, Crawford, E. D., additional, Cussenot, O., additional, Davis, F. G., additional, De Vivo, I., additional, Deng, X., additional, Ding, T., additional, Dinney, C. P., additional, Di Stefano, A. L., additional, Diver, W. R., additional, Duell, E. J., additional, Elena, J. W., additional, Fan, J.-H., additional, Feigelson, H. S., additional, Feychting, M., additional, Figueroa, J. D., additional, Flanagan, A. M., additional, Fraumeni, J. F., additional, Freedman, N. D., additional, Fridley, B. L., additional, Fuchs, C. S., additional, Gago-Dominguez, M., additional, Gallinger, S., additional, Gao, Y.-T., additional, Gapstur, S. M., additional, Garcia-Closas, M., additional, Garcia-Closas, R., additional, Gastier-Foster, J. M., additional, Gaziano, J. M., additional, Gerhard, D. S., additional, Giffen, C. A., additional, Giles, G. G., additional, Gillanders, E. M., additional, Giovannucci, E. L., additional, Goggins, M., additional, Gokgoz, N., additional, Goldstein, A. M., additional, Gonzalez, C., additional, Gorlick, R., additional, Greene, M. H., additional, Gross, M., additional, Grossman, H. B., additional, Grubb, R., additional, Gu, J., additional, Guan, P., additional, Haiman, C. A., additional, Hallmans, G., additional, Hankinson, S. E., additional, Harris, C. C., additional, Hartge, P., additional, Hattinger, C., additional, Hayes, R. B., additional, He, Q., additional, Helman, L., additional, Henderson, B. E., additional, Henriksson, R., additional, Hoffman-Bolton, J., additional, Hohensee, C., additional, Holly, E. A., additional, Hong, Y.-C., additional, Hoover, R. N., additional, Hosgood, H. D., additional, Hsiao, C.-F., additional, Hsing, A. W., additional, Hsiung, C. A., additional, Hu, N., additional, Hu, W., additional, Hu, Z., additional, Huang, M.-S., additional, Hunter, D. J., additional, Inskip, P. D., additional, Ito, H., additional, Jacobs, E. J., additional, Jacobs, K. B., additional, Jenab, M., additional, Ji, B.-T., additional, Johansen, C., additional, Johansson, M., additional, Johnson, A., additional, Kaaks, R., additional, Kamat, A. M., additional, Kamineni, A., additional, Karagas, M., additional, Khanna, C., additional, Khaw, K.-T., additional, Kim, C., additional, Kim, I.-S., additional, Kim, J. H., additional, Kim, Y. H., additional, Kim, Y.-C., additional, Kim, Y. T., additional, Kang, C. H., additional, Jung, Y. J., additional, Kitahara, C. M., additional, Klein, A. P., additional, Klein, R., additional, Kogevinas, M., additional, Koh, W.-P., additional, Kohno, T., additional, Kolonel, L. N., additional, Kooperberg, C., additional, Kratz, C. P., additional, Krogh, V., additional, Kunitoh, H., additional, Kurtz, R. C., additional, Kurucu, N., additional, Lan, Q., additional, Lathrop, M., additional, Lau, C. C., additional, Lecanda, F., additional, Lee, K.-M., additional, Lee, M. P., additional, Le Marchand, L., additional, Lerner, S. P., additional, Li, D., additional, Liao, L. M., additional, Lim, W.-Y., additional, Lin, D., additional, Lin, J., additional, Lindstrom, S., additional, Linet, M. S., additional, Lissowska, J., additional, Liu, J., additional, Ljungberg, B., additional, Lloreta, J., additional, Lu, D., additional, Ma, J., additional, Malats, N., additional, Mannisto, S., additional, Marina, N., additional, Mastrangelo, G., additional, Matsuo, K., additional, McGlynn, K. A., additional, McKean-Cowdin, R., additional, McNeill, L. H., additional, McWilliams, R. R., additional, Melin, B. S., additional, Meltzer, P. S., additional, Mensah, J. E., additional, Miao, X., additional, Michaud, D. S., additional, Mondul, A. M., additional, Moore, L. E., additional, Muir, K., additional, Niwa, S., additional, Olson, S. H., additional, Orr, N., additional, Panico, S., additional, Park, J. Y., additional, Patel, A. V., additional, Patino-Garcia, A., additional, Pavanello, S., additional, Peeters, P. H. M., additional, Peplonska, B., additional, Peters, U., additional, Petersen, G. M., additional, Picci, P., additional, Pike, M. C., additional, Porru, S., additional, Prescott, J., additional, Pu, X., additional, Purdue, M. P., additional, Qiao, Y.-L., additional, Rajaraman, P., additional, Riboli, E., additional, Risch, H. A., additional, Rodabough, R. J., additional, Rothman, N., additional, Ruder, A. M., additional, Ryu, J.-S., additional, Sanson, M., additional, Schned, A., additional, Schumacher, F. R., additional, Schwartz, A. G., additional, Schwartz, K. L., additional, Schwenn, M., additional, Scotlandi, K., additional, Seow, A., additional, Serra, C., additional, Serra, M., additional, Sesso, H. D., additional, Severi, G., additional, Shen, H., additional, Shen, M., additional, Shete, S., additional, Shiraishi, K., additional, Shu, X.-O., additional, Siddiq, A., additional, Sierrasesumaga, L., additional, Sierri, S., additional, Loon Sihoe, A. D., additional, Silverman, D. T., additional, Simon, M., additional, Southey, M. C., additional, Spector, L., additional, Spitz, M., additional, Stampfer, M., additional, Stattin, P., additional, Stern, M. C., additional, Stevens, V. L., additional, Stolzenberg-Solomon, R. Z., additional, Stram, D. O., additional, Strom, S. S., additional, Su, W.-C., additional, Sund, M., additional, Sung, S. W., additional, Swerdlow, A., additional, Tan, W., additional, Tanaka, H., additional, Tang, W., additional, Tang, Z.-Z., additional, Tardon, A., additional, Tay, E., additional, Taylor, P. R., additional, Tettey, Y., additional, Thomas, D. M., additional, Tirabosco, R., additional, Tjonneland, A., additional, Tobias, G. S., additional, Toro, J. R., additional, Travis, R. C., additional, Trichopoulos, D., additional, Troisi, R., additional, Truelove, A., additional, Tsai, Y.-H., additional, Tucker, M. A., additional, Tumino, R., additional, Van Den Berg, D., additional, Van Den Eeden, S. K., additional, Vermeulen, R., additional, Vineis, P., additional, Visvanathan, K., additional, Vogel, U., additional, Wang, C., additional, Wang, J., additional, Wang, S. S., additional, Weiderpass, E., additional, Weinstein, S. J., additional, Wentzensen, N., additional, Wheeler, W., additional, White, E., additional, Wiencke, J. K., additional, Wolk, A., additional, Wolpin, B. M., additional, Wong, M. P., additional, Wrensch, M., additional, Wu, C., additional, Wu, T., additional, Wu, X., additional, Wu, Y.-L., additional, Wunder, J. S., additional, Xiang, Y.-B., additional, Xu, J., additional, Yang, H. P., additional, Yang, P.-C., additional, Yatabe, Y., additional, Ye, Y., additional, Yeboah, E. D., additional, Yin, Z., additional, Ying, C., additional, Yu, C.-J., additional, Yu, K., additional, Yuan, J.-M., additional, Zanetti, K. A., additional, Zeleniuch-Jacquotte, A., additional, Zheng, W., additional, Zhou, B., additional, Mirabello, L., additional, Savage, S. A., additional, Kraft, P., additional, Chanock, S. J., additional, Yeager, M., additional, Landi, M. T., additional, Shi, J., additional, Chatterjee, N., additional, and Amundadottir, L. T., additional

Published
2014
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55. Early versus 6–12 week postpartum glucose tolerance testing for women with gestational diabetes

Author

Carter, E B, Martin, S, Temming, L A, Colditz, G A, Macones, G A, and Tuuli, M G

Abstract

Objective:The objective of this study is to estimate the accuracy of early oral glucose tolerance testing (GTT), to predict impaired glucose tolerance.Study Design:This was a prospective cohort study. Women received an early 75 g 2 h GTT between postpartum days 2–4 and again 6–12 weeks postpartum. The ability of the early GTT to accurately detect impaired glucose tolerance and diabetes was assessed by calculating sensitivity, specificity, positive predictive value (PPV) and negative predictive values (NPVs). The routine 6–12-week postpartum GTT was considered the gold standard.Results:The early GTT was completed by 100% of subjects, whereas only 31 of 58 (53%) women returned to complete the 6–12-week postpartum GTT. The early GTT had modest sensitivity for impaired glucose tolerance (62.5%) and overt diabetes (50%). However, it had excellent specificity (100%), PPV (100%) and NPV (96.7%) for diabetes. The NPV for impaired glucose tolerance with the early GTT was 80%.Conclusion:Rates of 6–12 week postpartum GTT completion among patients with gestational diabetes is poor. Appropriate postpartum management may improve by using the early GTT as a screening test.

Published
2018
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56. Alcohol, tobacco and breast cancer - collaborative reanalysis of individual data from 53 epidemiological studies, including 58515 women with breast cancer and 95067 women without the disease

Author

Beral, V Hamajima, N Hirose, K Rohan, T Calle, EE and Heath, CW Coates, RJ Liff, JM Talamini, R Chantarakul, N and Koetsawang, S Rachawat, D Morabia, A Schuman, L and Stewart, W Szklo, M Bain, C Schofield, F Siskind, V and Band, P Coldman, AJ Gallagher, RP Hislop, TG Yang, P and Kolonel, LM Nomura, AMY Hu, J Johnson, KC Mao, Y De Sanjose, S Lee, N Marchbanks, P Ory, HW Peterson, HB and Wilson, HG Wingo, PA Ebeling, K Kunde, D Nishan, P and Hopper, JL Colditz, G Gajalakshmi, V Martin, N and Pardthaisong, T Solpisornkosol, S Theetranont, C Boosiri, B and Chutivongse, S Jimakorn, P Virutamasen, P and Wongsrichanalai, C Ewertz, M Adami, HO Bergkvist, L and Magnusson, C Persson, I Chang-Claude, J Paul, C Skegg, DCG Spears, GFS Boyle, P Evstifeeva, T Daling, JR and Hutchinson, WB Malone, K Noonan, EA Stanford, JL Thomas, DB Weiss, NS White, E Andrieu, N Bremond, A Clavel, F Gairard, B Lansac, J Piana, L Renaud, R Izquierdo, A Viladiu, P Cuevas, HR Ontiveros, P Palet, A and Salazar, SB Arsitizabal, N Cuadros, A Tryggvadottir, L and Tulinius, H Bachelot, A Le, MG Peto, J Franceschi, S and Lubin, F Modan, B Ron, E Wax, Y Friedman, GD Hiatt, RA Levi, F Bishop, T Kosmelj, K Primic-Zakelj, M and Ravnihar, B Stare, J Beeson, WL Fraser, G Bulbrook, RD and Cuzick, J Duffy, SW Fentiman, IS Hayward, JL Wang, DY McMichael, AJ McPherson, K Hanson, RL Leske, MC and Mahoney, MC Nasca, PC Varma, AO Weinstein, AL Moller, TR and Olsson, H Ranstam, J Goldbohm, RA van den Brandt, PA and Apelo, RA Baens, J de la Cruz, JR Javier, B Lacaya, LB and Ngelangel, CA La Vecchia, C Negri, E Marubini, E and Ferraroni, M Gerber, M Richardson, S Segala, C Gatei, D and Kenya, P Kungu, A Mati, JG Brinton, LA Hoover, R and Schairer, C Spirtas, R Lee, HP Rookus, MA van Leeuwen, FE Schoenberg, JA McCredie, M Gammon, MD Clarke, EA and Jones, L Neil, A Vessey, M Yeates, D Appleby, P and Banks, E Bull, D Crossley, B Goodill, A Green, J and Hermon, C Key, T Langston, N Lewis, C Reeves, G and Collins, R Doll, R Peto, R Mabuchi, K Preston, D and Hannaford, P Kay, C Rosero-Bixby, L Gao, YT Jin, F and Yuan, JM Wei, HY Yun, T Zhiheng, C Berry, G Cooper Booth, J Jelihovsky, T MacLennan, R Shearman, R Wang, QS and Baines, CJ Miller, AB Wall, C Lund, E Stalsberg, H and Shu, XO Zheng, W Katsouyanni, K Trichopoulou, A and Trichopoulos, D Dabancens, A Martinez, L Molina, R and Salas, O Alexander, XE Anderson, K Folsom, AR Hulka, BS and Bernstein, L Enger, S Haile, RW Paganini-Hill, A and Pike, MC Ross, RK Ursin, G Yu, MC Longnecker, MP and Newcomb, P Bergkvist, L Kalache, A Farley, TMM Holck, S and Meirik, O Collaborative Group on Hormonal Factors in Breast Cancer

Abstract

Alcohol and tobacco consumption are closely correlated and published results on their association with breast cancer have not always allowed adequately for confounding between these exposures. Over 80% of the relevant information worldwide on alcohol and tobacco consumption and breast cancer were collated, checked and analysed centrally. Analyses included 58515 women with invasive breast cancer and 95067 controls from 53 studies. Relative risks of breast cancer were estimated, after stratifying by study, age, parity and, where appropriate, women’s age when their first child was born and consumption of alcohol and tobacco. The average consumption of alcohol reported by controls from developed countries was 6.0 g per day, i.e. about half a unit/drink of alcohol per day, and was greater in ever-smokers than never-smokers, (8.4 g per day and 5.0 g per day, respectively). Compared with women who reported drinking no alcohol, the relative risk of breast cancer was 1.32 (1.19 - 1.45, P < 0.00001) for an intake of 35 - 44 g per day alcohol, and 1.46 (1.33 - 1.61, P < 0.00001) for greater than or equal to 45 g per day alcohol. The relative risk of breast cancer increased by 7.1% (95% CI 5.5-8.7%; P

Published
2002

57. Differentially expressed genes regulating the progression of ductal carcinoma in situ to invasive breast cancer

Author

Lee, S., Stewart, S., Nagtegaal, I.D., Luo, J., Wu, Y., Colditz, G., Medina, D., Allred, D.C., Lee, S., Stewart, S., Nagtegaal, I.D., Luo, J., Wu, Y., Colditz, G., Medina, D., and Allred, D.C.

Abstract

Contains fulltext : 110917pub.pdf (publisher's version ) (Closed access), Molecular mechanisms mediating the progression of ductal carcinoma in situ (DCIS) to invasive breast cancer remain largely unknown. We used gene expression profiling of human DCIS (n = 53) and invasive breast cancer (n = 51) to discover uniquely expressed genes that may also regulate progression. There were 470 total differentially expressed genes (>/=2-fold; P < 0.05). Elevated expression of genes involved in synthesis and organization of extracellular matrix was particularly prominent in the epithelium of invasive breast cancer. The degree of overlap of the genes with nine similar studies in the literature was determined to help prioritize their potential importance, resulting in 74 showing overlap in >/=2 studies (average 3.6 studies/gene; range 2-8 studies). Using hierarchical clustering, the 74-gene profile correctly categorized 96% of samples in this study and 94% of samples from 3 similar independent studies. To study the progression of DCIS to invasive breast cancer in vivo, we introduced human DCIS cell lines engineered to express specific genes into a "mammary intraductal DCIS" xenograft model. Progression of xenografts to invasive breast cancer was dramatically increased by suppressing four genes that were usually elevated in clinical samples of DCIS, including a protease inhibitor (CSTA) and genes involved in cell adhesion and signaling (FAT1, DST, and TMEM45A), strongly suggesting that they normally function to suppress progression. In summary, we have identified unique gene expression profiles of human DCIS and invasive breast cancer, which include novel genes regulating tumor progression. Targeting some of these genes may improve the detection, diagnosis, and therapy of DCIS.

Published
2012

61. A pooled analysis of 12 cohort studies of dietary fat, cholesterol and egg intake and ovarian cancer

Author

Genkinger, J M, Hunter, D J, Spiegelman, D, Anderson, K E, Beeson, W L, Buring, J E, Colditz, G A, Fraser, G E, Freudenheim, J L, Goldbohm, R A, Hankinson, S E, Koenig, K L, Larsson, S C, Leitzmann, M, McCullough, M L, Miller, A B, Rodriguez, C, Rohan, T E, Ross, J A, Schatzkin, A, Schouten, L J, Smit, E, Willett, W C, Wolk, A, Zeleniuch-Jacquotte, A, Zhang, S M M, Smith-Warner, S, Genkinger, J M, Hunter, D J, Spiegelman, D, Anderson, K E, Beeson, W L, Buring, J E, Colditz, G A, Fraser, G E, Freudenheim, J L, Goldbohm, R A, Hankinson, S E, Koenig, K L, Larsson, S C, Leitzmann, M, McCullough, M L, Miller, A B, Rodriguez, C, Rohan, T E, Ross, J A, Schatzkin, A, Schouten, L J, Smit, E, Willett, W C, Wolk, A, Zeleniuch-Jacquotte, A, Zhang, S M M, and Smith-Warner, S

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.

Published
2006
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62. Haplotype analysis of the HSD17B1 gene and risk of breast cancer: a comprehensive approach to multicenter analyses of prospective cohort studies.

Author

Feigelson, H.S., Cox, D.G., Cann, H.M., Wacholder, S., Kaaks, R., Henderson, B.E., Albanes, D., Altshuler, D., Berglund, G., Berrino, F., Bingham, S, Buring, J.E., Burtt, N.P., Calle, E.E., Chanock, S.J., Clavel-Chapelon, F., Colditz, G., Diver, W.R., Freedman, M.L., Haiman, C.A., Hankinson, S.E., Hayes, R.B., Hirschhorn, J.N., Hunter, D., Kolonel, L.N., Kraft, P., LeMarchand, L., Linseisen, J., Modi, W., Navarro, C., Peeters, P.H.M., Pike, M.C., Riboli, E., Setiawan, V.W., Stram, D.O., Thomas, G., Thun, M.J., Tjonneland, A., Trichopoulos, D., Feigelson, H.S., Cox, D.G., Cann, H.M., Wacholder, S., Kaaks, R., Henderson, B.E., Albanes, D., Altshuler, D., Berglund, G., Berrino, F., Bingham, S, Buring, J.E., Burtt, N.P., Calle, E.E., Chanock, S.J., Clavel-Chapelon, F., Colditz, G., Diver, W.R., Freedman, M.L., Haiman, C.A., Hankinson, S.E., Hayes, R.B., Hirschhorn, J.N., Hunter, D., Kolonel, L.N., Kraft, P., LeMarchand, L., Linseisen, J., Modi, W., Navarro, C., Peeters, P.H.M., Pike, M.C., Riboli, E., Setiawan, V.W., Stram, D.O., Thomas, G., Thun, M.J., Tjonneland, A., and Trichopoulos, D.

Published
2006

63. Haplotype analysis of the HSD17B1 gene and risk of breast cancer: a comprehensive approach to multicenter analyses of prospective cohort studies.

Author

JC onderzoeksprogramma Kanker, Epidemiology & Health Economics, Feigelson, H.S., Cox, D.G., Cann, H.M., Wacholder, S., Kaaks, R., Henderson, B.E., Albanes, D., Altshuler, D., Berglund, G., Berrino, F., Bingham, S, Buring, J.E., Burtt, N.P., Calle, E.E., Chanock, S.J., Clavel-Chapelon, F., Colditz, G., Diver, W.R., Freedman, M.L., Haiman, C.A., Hankinson, S.E., Hayes, R.B., Hirschhorn, J.N., Hunter, D., Kolonel, L.N., Kraft, P., LeMarchand, L., Linseisen, J., Modi, W., Navarro, C., Peeters, P.H.M., Pike, M.C., Riboli, E., Setiawan, V.W., Stram, D.O., Thomas, G., Thun, M.J., Tjonneland, A., Trichopoulos, D., JC onderzoeksprogramma Kanker, Epidemiology & Health Economics, Feigelson, H.S., Cox, D.G., Cann, H.M., Wacholder, S., Kaaks, R., Henderson, B.E., Albanes, D., Altshuler, D., Berglund, G., Berrino, F., Bingham, S, Buring, J.E., Burtt, N.P., Calle, E.E., Chanock, S.J., Clavel-Chapelon, F., Colditz, G., Diver, W.R., Freedman, M.L., Haiman, C.A., Hankinson, S.E., Hayes, R.B., Hirschhorn, J.N., Hunter, D., Kolonel, L.N., Kraft, P., LeMarchand, L., Linseisen, J., Modi, W., Navarro, C., Peeters, P.H.M., Pike, M.C., Riboli, E., Setiawan, V.W., Stram, D.O., Thomas, G., Thun, M.J., Tjonneland, A., and Trichopoulos, D.

Published
2006

64. Alcohol and postmenopausal breast cancer risk defined by estrogen and progesterone receptor status : A prospective cohort study

Author

Suzuki, R, Ye, W M, Rylander-Rudqvist, T, Saji, S, Colditz, G A, Wolk, A, Suzuki, R, Ye, W M, Rylander-Rudqvist, T, Saji, S, Colditz, G A, and Wolk, A

Abstract

Background: Alcohol intake has been reported to be positively associated with an increased risk of postmenopausal breast cancer; however, the association with the estrogen receptor (ER) and progesterone receptor (PR) status of the breast tumors remains unclear. Methods: Self-reported data on alcohol consumption were collected in 1987 and 1997 from 51847 postmenopausal women in the population-based Swedish Mammography Cohort. Through June 30,2004,1188 invasive breast cancer case patients with known ER and PR status were identified during an average 8.3-year follow-up. We used Cox proportional hazards models to estimate multivariable relative risks (RRs) of breast cancer, adjusting for age; family history of breast cancer; body mass index; height; parity; age at menarche, first birth, and menopause; education level; use of postmenopausal hormones; and diet. Heterogeneity among groups was evaluated using the Wald test. All statistical tests were two-sided. Results: Alcohol consumption was associated with an increased risk for the development of ER-positive (+) tumors, irrespective of PR status (highest intake [ >= 10 g of alcohol per day] versus nondrinkers, multivariable RR = 1.35, 95% confidence interval [CI] = 1.02 to 1.80; P-trend < .049 for ER+PR+ tumors; and RR = 2.36, 95% CI = 1.56 to 3.56; P-trend < .001 for ER+PR-tumors). The absolute rate of ER+ breast cancer (standardized to the age distribution of person-years experienced by all study participants using 5-year age categories) was 232 per 100000 person-years among women in the highest category of alcohol intake, and 158 per 100000 person-years among nondrinkers. No association was observed between alcohol intake and the risk of developing ER-tumors. Furthermore, we observed a statistically significant interaction between alcohol intake and the use of postmenopausal hormones on the risk for ER+PR+ tumors (P-interaction = .039). Conclusion: The observed association between risk of developing postmenop

Published
2005
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65. Fruits and vegetables and ovarian cancer risk in a pooled analysis of 12 cohort studies

Author

Koushik, A, Hunter, D J, Spiegelman, D, Anderson, K E, Arslan, A A, Beeson, W L, van den Brandt, P A, Buring, J E, Cerhan, J R, Colditz, G A, Fraser, G E, Freudenheim, J L, Genkinger, J M, Goldbohm, R A, Hankinson, S E, Koenig, K L, Larsson, S C, Leitzmann, M, McCullough, M L, Miller, A B, Patel, A, Rohan, T E, Schatzkin, A, Smit, E, Willett, W C, Wolk, A, Zhang, S M M, Smith-Warner, S A, Koushik, A, Hunter, D J, Spiegelman, D, Anderson, K E, Arslan, A A, Beeson, W L, van den Brandt, P A, Buring, J E, Cerhan, J R, Colditz, G A, Fraser, G E, Freudenheim, J L, Genkinger, J M, Goldbohm, R A, Hankinson, S E, Koenig, K L, Larsson, S C, Leitzmann, M, McCullough, M L, Miller, A B, Patel, A, Rohan, T E, Schatzkin, A, Smit, E, Willett, W C, Wolk, A, Zhang, S M M, and Smith-Warner, S A

Abstract

Because fruits and vegetables are rich in bioactive compounds with potential cancer-preventive actions, increased consumption may reduce the risk of ovarian cancer. Evidence on the association between fruit and vegetable intake and ovarian cancer risk has not been consistent. We analyzed and pooled the primary data from 12 prospective studies in North America and Europe. Fruit and vegetable intake was measured at baseline in each study using a validated food frequency questionnaire. To summarize the association between fruit and vegetable intake and ovarian cancer, study-specific relative risks (RR) were estimated using the Cox proportional hazards model, and then combined using a random-effects model. Among 560,441 women, 2,130 cases of invasive epithelial ovarian cancer occurred during a maximum follow-up of 7 to 22 years across studies. Total fruit intake was not associated with ovarian cancer risk-the pooled multivariate RR for the highest versus the lowest quartile of intake was 1.06 [95% confidence interval (95% CI), 0.92-1.21; P value, test for trend = 0.73; P value, test for between-studies heterogeneity = 0.741. Similarly, results for total vegetable intake indicated no significant association (pooled multivariate RR, 0.90; 95% Cl, 0.78-1.04, for the highest versus the lowest quartile; P value, test for trend = 0.06; P value, test for between-studies heterogeneity = 0.31). Intakes of botanically defined fruit and vegetable groups and individual fruits and vegetables were also not associated with ovarian cancer risk. Associations for total fruits and vegetables were similar for different histologic types. These results suggest that fruit and vegetable consumption in adulthood has no important association with the risk of ovarian cancer.

Published
2005
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66. Alcohol consumption and risk of lung cancer: a pooled analysis of cohort studies

Author

Freudenheim, J.L., Freudenheim, J.L., Ritz, J., Smith Warner, S.A., Albanes, D., Bandera, E.V., van den Brandt, P.A., Colditz, G., Feskanich, D., Goldbohm, R.A., Harnack, L., Miller, A.B., Rimm, E., Rohan, T.E., Sellers, T.A., Virtamo, J., Willett, W.C., Hunter, D.J., Freudenheim, J.L., Freudenheim, J.L., Ritz, J., Smith Warner, S.A., Albanes, D., Bandera, E.V., van den Brandt, P.A., Colditz, G., Feskanich, D., Goldbohm, R.A., Harnack, L., Miller, A.B., Rimm, E., Rohan, T.E., Sellers, T.A., Virtamo, J., Willett, W.C., and Hunter, D.J.

Abstract

BACKGROUND: Although smoking is the primary cause of lung cancer, much is unknown about lung cancer etiology, including risk determinants for nonsmokers and modifying factors for smokers. OBJECTIVE: We hypothesized that alcohol consumption contributes to lung cancer risk. DESIGN: We conducted a pooled analysis using standardized exposure and covariate data from 7 prospective studies with 399,767 participants and 3137 lung cancer cases. Study-specific relative risks (RRs) and CIs were estimated and then combined to calculate pooled multivariate RRs by using a random-effects model. RESULTS: We found a slightly greater risk for the consumption of > or = 30 g alcohol/d than for that of 0 g alcohol/d in men (RR: 1.21; 95% CI: 0.91, 1.61; P for trend = 0.03) and in women (RR: 1.16; 95% CI: 0.94, 1.43; P for trend = 0.03). In male never smokers, the RR for consumption of > or = 15 g alcohol/d rather than 0 g alcohol/d was 6.38 (95% CI: 2.74, 14.9; P for trend < 0.001). In women, there were few never-smoking cases and no evidence of greater risk (RR: 1.35; 95% CI: 0.64, 2.87). Because of possible residual confounding by smoking, we performed sensitivity analyses by reclassifying the never smokers in the highest drinking category as former smokers. Resulting associations for alcohol consumption were somewhat attenuated, but P for trend = 0.05 for men, which was near the original P = 0.03. CONCLUSIONS: A slightly greater risk of lung cancer was associated with the consumption of > or = 30 g alcohol/d than with no alcohol consumption. Alcohol consumption was strongly associated with greater risk in male never smokers. Residual confounding by smoking may explain part of the observed relation.

Published
2005

69. Dairy foods, calcium, and colorectal cancer : A pooled analysis of 10 cohort studies

Author

Cho, E, Smith-Warner, S A, Spiegelman, D, Beeson, W L, van den Brandt, P A, Colditz, G A, Folsom, A R, Fraser, G E, Freudenheim, J L, Giovannucci, E, Goldbohm, R A, Graham, S, Miller, A B, Pietinen, P, Potter, J D, Rohan, T E, Terry, P, Toniolo, P, Virtanen, M J, Willett, W C, Wolk, A, Wu, K, Yaun, S S, Zeleniuch-Jacquotte, A, Hunter, D J, Cho, E, Smith-Warner, S A, Spiegelman, D, Beeson, W L, van den Brandt, P A, Colditz, G A, Folsom, A R, Fraser, G E, Freudenheim, J L, Giovannucci, E, Goldbohm, R A, Graham, S, Miller, A B, Pietinen, P, Potter, J D, Rohan, T E, Terry, P, Toniolo, P, Virtanen, M J, Willett, W C, Wolk, A, Wu, K, Yaun, S S, Zeleniuch-Jacquotte, A, and Hunter, D J

Abstract

Background. Studies in animals have suggested that calcium may reduce the risk of colorectal cancer. However, results from epidemiologic studies of intake of calcium or dairy foods and colorectal cancer risk have been inconclusive. Methods: We pooled the primary data from 10 cohort studies in five countries that assessed usual dietary intake by using a validated food frequency questionnaire at baseline. For most studies, follow-up was extended beyond that in the original publication. The studies included 534 536 individuals, among whom 4992 incident cases of colorectal cancer were diagnosed between 6 and 16 years of follow-up. Pooled multivariable relative risks for categories of milk intake and quintiles of calcium intake and 95% confidence intervals (CIs) were calculated. All statistical tests were two-sided. Results: Milk intake was related to a reduced risk of colorectal cancer. Compared with the lowest category of intake (<70 g/day), relative risks of colorectal cancer for increasing categories (70-174, 175-249, and greater than or equal to250 g/day) of milk intake were 0.94 (95% CI = 0.86 to 1.02), 0.88 (95% CI = 0.81 to 0.96), and 0.85 (95% CI = 0.78 to 0.94), respectively (P-trend<.001). Calcium intake was also inversely related to the risk of colorectal cancer. The relative risk for the highest versus the lowest quintile of intake was 0.86 (95% CI = 0.78 to 0.95; P-trend = .02) for dietary calcium and 0.78 (95% CI = 0.69 to 0.88; P-trend<.001) for total calcium (combining dietary and supplemental sources). These results were consistent across studies and sex. The inverse association for milk was limited to cancers of the distal colon (P-trend<.001) and rectum (P-trend = .02). Conclusion: Higher consumption of milk and calcium is associated with a lower risk of colorectal cancer.

Published
2004
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70. Dietary Carotenoids and Risk of Lung Cancer in a Pooled Analysis of Seven Cohort Studies

Author

Männistö, S., Smith-Warner, S.A., Spiegelman, D., Albanes, D., Anderson, K., Brandt, P.A. van den, Cerhan, J.R., Colditz, G., Feskanich, D., Freudenheim, J.L., Giovannucci, E., Goldbohm, R.A., Graham, S., Miller, A.B., Rohan, T.E., Virtamo, J., Willett, W.C., Hunter, D.J., Männistö, S., Smith-Warner, S.A., Spiegelman, D., Albanes, D., Anderson, K., Brandt, P.A. van den, Cerhan, J.R., Colditz, G., Feskanich, D., Freudenheim, J.L., Giovannucci, E., Goldbohm, R.A., Graham, S., Miller, A.B., Rohan, T.E., Virtamo, J., Willett, W.C., and Hunter, D.J.

Abstract

Intervention trials with supplemental β-carotene have observed either no effect or a harmful effect on lung cancer risk. Because food composition databases for specific carotenoids have only become available recently, epidemiological evidence relating usual dietary levels of these carotenoids with lung cancer risk is limited. We analyzed the association between lung cancer risk and intakes of specific carotenoids using the primary data from seven cohort studies in North America and Europe. Carotenoid intakes were estimated from dietary questionnaires administered at baseline in each study. We calculated study-specific multivariate relative risks (RRs) and combined these using a random-effects model. The multivariate models included smoking history and other potential risk factors. During follow-up of up to 7-16 years across studies, 3,155 incident lung cancer cases were diagnosed among 399,765 participants. β-Carotene intake was not associated with lung cancer risk (pooled multivariate RR = 0.98; 95% confidence interval, 0.87-1.11; highest versus lowest quintile). The RRs for α-carotene, lutein/zeaxanthin, and lycopene were also close to unity. β-Cryptoxanthin intake was inversely associated with lung cancer risk (RR = 0.76; 95% confidence interval, 0.67-0. 86; highest versus lowest quintile). These results did not change after adjustment for intakes of vitamin C (with or without supplements), folate (with or without supplements), and other carotenoids and multivitamin use. The associations generally were similar among never, past, or current smokers and by histological type. Although smoking is the strongest risk factor for lung cancer, greater intake of foods high in β-cryptoxanthin, such as citrus fruit, may modestly lower the risk.

Published
2004

79. Alcohol, tobacco and breast cancer--collaborative reanalysis of individualdata from 53 epidemiological studies, including 58,515 women with breastcancer and 95,067 women without the disease.

Author

Hamajima, N, Hirose, K, Tajima, K, Rohan, T, Calle, EE, Heath CW, Jr, Coates, RJ, Liff, JM, Talamini, R, Chantarakul, N, Koetsawang, S, Rachawat, D, Morabia, A, Schuman, L, Stewart, W, Szklo, M, Bain, C, Schofield, F, Siskind, V, Band, P, Coldman, AJ, Gallagher, RP, Hislop, TG, Yang, P, Kolonel, LM, Nomura, AM, Hu, J, Johnson, KC, Mao, Y, De Sanjose, S, Lee, N, Marchbanks, P, Ory, HW, Peterson, HB, Wilson, HG, Wingo, PA, Ebeling, K, Kunde, D, Nishan, P, Hopper, JL, Colditz, G, Gajalanski, V, Martin, N, Pardthaisong, T, Silpisornkosol, S, Theetranont, C, Boosiri, B, Chutivongse, S, Jimakorn, P, Virutamasen, P, Wongsrichanalai, C, Ewertz, M, Adami, HO, Bergkvist, L, Magnusson, C, Persson, I, Chang-Claude, J, Paul, C, Skegg, DC, Spears, GF, Boyle, P, Evstifeeva, T, Daling, JR, Hutchinson, WB, Malone, K, Noonan, EA, Stanford, JL, Thomas, DB, Weiss, NS, White, E, Andrieu, N, Bremond, A, Clavel, F, Gairard, B, Lansac, J, Piana, L, Renaud, R, Izquierdo, A, Viladiu, P, Cuevas, HR, Ontiveros, P, Palet, A, Salazar, SB, Aristizabel, N, Cuadros, A, Tryggvadottir, L, Tulinius, H, Bachelot, A, Le, MG, Peto, J, Franceschi, S, Lubin, F, Modan, B, Ron, E, Wax, Y, Friedman, GD, Hiatt, RA, Levi, F, Bishop, T, Kosmelj, K, Primic-Zakelj, M, Ravnihar, B, Stare, J, Beeson, WL, Fraser, G, Bullbrook, RD, Cuzick, J, Duffy, SW, Fentiman, IS, Hayward, JL, Wang, DY, McMichael, AJ, McPherson, K, Hanson, RL, Leske, MC, Mahoney, MC, Nasca, PC, Varma, AO, Weinstein, AL, Moller, TR, Olsson, H, Ranstam, J, Goldbohm, RA, van den Brandt, PA, Apelo, RA, Baens, J, de la Cruz, JR, Javier, B, Lacaya, LB, Ngelangel, CA, La Vecchia, C, Negri, E, Marubini, E, Ferraroni, M, Gerber, M, Richardson, S, Segala, C, Gatei, D, Kenya, P, Kungu, A, Mati, JG, Brinton, LA, Hoover, R, Schairer, C, Spirtas, R, Lee, HP, Rookus, MA, van Leeuwen, FE, Schoenberg, JA, McCredie, M, Gammon, MD, Clarke, EA, Jones, L, Neil, A, Vessey, M, Yeates, D, Appleby, P, Banks, E, Beral, V, Bull, D, Crossley, B, Goodill, A, Green, J, Hermon, C, Key, T, Langston, N, Lewis, C, Reeves, G, Collins, R, Doll, R, Peto, R, Mabuchi, K, Preston, D, Hannaford, P, Kay, C, Rosero-Bixby, L, Gao, YT, Jin, F, Yuan, JM, Wei, HY, Yun, T, Zhiheng, C, Berry, G, Cooper Booth, J, Jelihovsky, T, MacLennan, R, Shearman, R, Wang, QS, Baines, CJ, Miller, AB, Wall, C, Lund, E, Stalsberg, H, Shu, XO, Zheng, W, Katsouyanni, K, Trichopoulou, A, Trichopoulos, D, Dabancens, A, Martinez, L, Molina, R, Salas, O, Alexander, FE, Anderson, K, Folsom, AR, Hulka, BS, Bernstein, L, Enger, S, Haile, RW, Paganini-Hill, A, Pike, MC, Ross, RK, Ursin, G, Yu, MC, Longnecker, MP, Newcomb, P, Kalache, A, Farley, TM, Holck, S, Meirik, O, Hamajima, N, Hirose, K, Tajima, K, Rohan, T, Calle, EE, Heath CW, Jr, Coates, RJ, Liff, JM, Talamini, R, Chantarakul, N, Koetsawang, S, Rachawat, D, Morabia, A, Schuman, L, Stewart, W, Szklo, M, Bain, C, Schofield, F, Siskind, V, Band, P, Coldman, AJ, Gallagher, RP, Hislop, TG, Yang, P, Kolonel, LM, Nomura, AM, Hu, J, Johnson, KC, Mao, Y, De Sanjose, S, Lee, N, Marchbanks, P, Ory, HW, Peterson, HB, Wilson, HG, Wingo, PA, Ebeling, K, Kunde, D, Nishan, P, Hopper, JL, Colditz, G, Gajalanski, V, Martin, N, Pardthaisong, T, Silpisornkosol, S, Theetranont, C, Boosiri, B, Chutivongse, S, Jimakorn, P, Virutamasen, P, Wongsrichanalai, C, Ewertz, M, Adami, HO, Bergkvist, L, Magnusson, C, Persson, I, Chang-Claude, J, Paul, C, Skegg, DC, Spears, GF, Boyle, P, Evstifeeva, T, Daling, JR, Hutchinson, WB, Malone, K, Noonan, EA, Stanford, JL, Thomas, DB, Weiss, NS, White, E, Andrieu, N, Bremond, A, Clavel, F, Gairard, B, Lansac, J, Piana, L, Renaud, R, Izquierdo, A, Viladiu, P, Cuevas, HR, Ontiveros, P, Palet, A, Salazar, SB, Aristizabel, N, Cuadros, A, Tryggvadottir, L, Tulinius, H, Bachelot, A, Le, MG, Peto, J, Franceschi, S, Lubin, F, Modan, B, Ron, E, Wax, Y, Friedman, GD, Hiatt, RA, Levi, F, Bishop, T, Kosmelj, K, Primic-Zakelj, M, Ravnihar, B, Stare, J, Beeson, WL, Fraser, G, Bullbrook, RD, Cuzick, J, Duffy, SW, Fentiman, IS, Hayward, JL, Wang, DY, McMichael, AJ, McPherson, K, Hanson, RL, Leske, MC, Mahoney, MC, Nasca, PC, Varma, AO, Weinstein, AL, Moller, TR, Olsson, H, Ranstam, J, Goldbohm, RA, van den Brandt, PA, Apelo, RA, Baens, J, de la Cruz, JR, Javier, B, Lacaya, LB, Ngelangel, CA, La Vecchia, C, Negri, E, Marubini, E, Ferraroni, M, Gerber, M, Richardson, S, Segala, C, Gatei, D, Kenya, P, Kungu, A, Mati, JG, Brinton, LA, Hoover, R, Schairer, C, Spirtas, R, Lee, HP, Rookus, MA, van Leeuwen, FE, Schoenberg, JA, McCredie, M, Gammon, MD, Clarke, EA, Jones, L, Neil, A, Vessey, M, Yeates, D, Appleby, P, Banks, E, Beral, V, Bull, D, Crossley, B, Goodill, A, Green, J, Hermon, C, Key, T, Langston, N, Lewis, C, Reeves, G, Collins, R, Doll, R, Peto, R, Mabuchi, K, Preston, D, Hannaford, P, Kay, C, Rosero-Bixby, L, Gao, YT, Jin, F, Yuan, JM, Wei, HY, Yun, T, Zhiheng, C, Berry, G, Cooper Booth, J, Jelihovsky, T, MacLennan, R, Shearman, R, Wang, QS, Baines, CJ, Miller, AB, Wall, C, Lund, E, Stalsberg, H, Shu, XO, Zheng, W, Katsouyanni, K, Trichopoulou, A, Trichopoulos, D, Dabancens, A, Martinez, L, Molina, R, Salas, O, Alexander, FE, Anderson, K, Folsom, AR, Hulka, BS, Bernstein, L, Enger, S, Haile, RW, Paganini-Hill, A, Pike, MC, Ross, RK, Ursin, G, Yu, MC, Longnecker, MP, Newcomb, P, Kalache, A, Farley, TM, Holck, S, and Meirik, O

Published
2002

80. Dietary fat and risk of lung cancer in a pooled analysis of prospective studies

Author

Smith-Warner, S.A., Smith-Warner, S.A., Ritz, J., Hunter, D.J., Albanes, D., Beeson, W.L., van den Brandt, P.A., Colditz, G., Folsom, A.R., Fraser, G., Freudenheim, J.L., Giovannucci, E., Goldbohm, R.A., Graham, S., Kushi, L., Miller, A.B., Rohan, T., Speizer, F.E., Virtamo, J., Willett, W.C., Smith-Warner, S.A., Smith-Warner, S.A., Ritz, J., Hunter, D.J., Albanes, D., Beeson, W.L., van den Brandt, P.A., Colditz, G., Folsom, A.R., Fraser, G., Freudenheim, J.L., Giovannucci, E., Goldbohm, R.A., Graham, S., Kushi, L., Miller, A.B., Rohan, T., Speizer, F.E., Virtamo, J., and Willett, W.C.

Abstract

Harvard School of Public Health, Department of Nutrition, Boston, Massachusetts 02115, USA. Lung cancer rates are highest in countries with the greatest fat intakes. In several case-control studies, positive associations have been observed between lung cancer and intakes of total and saturated fat, particularly among nonsmokers. We analyzed the association between fat and cholesterol intakes and lung cancer risk in eight prospective cohort studies that met predefined criteria. Among the 280,419 female and 149,862 male participants who were followed for up to 6-16 years, 3,188 lung cancer cases were documented. Using the Cox proportional hazards model, we calculated study-specific relative risks that were adjusted for smoking history and other potential risk factors. Pooled relative risks were computed using a random effects model. Fat intake was not associated with lung cancer risk. For an increment of 5% of energy from fat, the pooled multivariate relative risks were 1.01 [95% confidence interval (CI), 0.98-1.05] for total, 1.03 (95% CI, 0.96-1.11) for saturated, 1.01 (95% CI, 0.93-1.10) for monounsaturated, and 0.99 (95% CI, 0.90-1.10) for polyunsaturated fat. No associations were observed between intakes of total or specific types of fat and lung cancer risk among never, past, or current smokers. Dietary cholesterol was not associated with lung cancer incidence [for a 100-mg/day increment, the pooled multivariate relative risk was 1.01 (95% CI, 0.97-1.05)]. There was no statistically significant heterogeneity among studies or by sex. These data do not support an important relation between fat or cholesterol intakes and lung cancer risk. The means to prevent this important disease remains avoidance of smoking.

Published
2002

98. Comparative effectiveness on survival of zoledronic acid versus pamidronate in multiple myeloma.

Author

Sanfilippo, K. M., Gage, B., Luo, S., Weilbaecher, K., Tomasson, M., Vij, R., Colditz, G., and Carson, K.

Subjects
ZOLEDRONIC acid, DISODIUM pamidronate, MULTIPLE myeloma treatment, DRUG side effects, AMERICAN veterans
Abstract

Zoledronic acid and pamidronate are the two bisphosphonates approved in the United States to reduce multiple myeloma skeletal complications. Little prior evidence exists comparing survival outcomes between the two. We evaluated the incidence of skeletal-related events and overall survival in patients with myeloma treated with zoledronic acid versus pamidronate using a cohort of 1018 United States veterans. At a median follow-up of 26.9 months, patients receiving zoledronic acid had a 22% reduction in risk of death compared to pamidronate (hazard ratio 0.78; 95% confidence interval, 0.67-0.92). The benefit persisted after controlling for potential confounders. Adjusted Cox modeling with inverse probability weighting and propensity score matching supported these findings. Zoledronic acid was also associated with a 25% decrease in skeletal-related events. Zoledronic acid is associated with increased overall survival and decreased skeletal-related events compared to pamidronate in patients with multiple myeloma and should become the preferred bisphosphonate. [ABSTRACT FROM AUTHOR]

Published
2015
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100. Dietary Carotenoids and Risk of Colorectal Cancer in a Pooled Analysis of 11 Cohort Studies

Author

Mannisto, S., primary, Yaun, S.-S., additional, Hunter, D. J., additional, Spiegelman, D., additional, Adami, H.-O., additional, Albanes, D., additional, van den Brandt, P. A., additional, Buring, J. E., additional, Cerhan, J. R., additional, Colditz, G. A., additional, Freudenheim, J. L., additional, Fuchs, C. S., additional, Giovannucci, E., additional, Goldbohm, R. A., additional, Harnack, L., additional, Leitzmann, M., additional, McCullough, M. L., additional, Miller, A. B., additional, Rohan, T. E., additional, Schatzkin, A., additional, Virtamo, J., additional, Willett, W. C., additional, Wolk, A., additional, Zhang, S. M., additional, and Smith-Warner, S. A., additional

Published
2006
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