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1. Building a multigenic model of breast cancer susceptibility: CYP17 and HSD17B1 are two important candidates.

Author

Feigelson, H S, McKean-Cowdin, R, Coetzee, G A, Stram, D O, Kolonel, L N, and Henderson, B E

Abstract

We conducted a nested case-control study to evaluate whether polymorphisms in two genes involved in estrogen metabolism, CYP17 and HSD17B1, were useful in developing a breast cancer risk model that could help discriminate women who are at higher risk of breast cancer. If polymorphisms in these genes affect the level of circulating estrogens, they may directly influence breast cancer risk. The base population for this study is a multiethnic cohort study that includes African-American, Non-Latina White, Japanese, Latina, and Native Hawaiian women. For this analysis, 1508 randomly selected controls and 850 incident breast cancer cases of the first four ethnic groups who agreed to provide a blood specimen were included (76 and 80% response rates, respectively). The CYP17 A2 allele and the HSD17B1 A allele were considered "high-risk" alleles. Subjects were then classified according to number of high-risk alleles. After adjusting for age, weight, and ethnicity, we found that carrying one or more high-risk alleles increases the risk of advanced breast cancer in a dose-response fashion. The risk among women carrying four high-risk alleles was 2.21 [95% confidence interval (CI), 0.98-5.00; P for trend = 0.03] compared with those who carried none. This risk was largely limited to women who were not taking hormone replacement therapy (relative risk, 2.60; 95% CI, 0.95-7.14) and was most pronounced among those weighing 170 pounds or less (RR, 3.05; 95% CI, 1.29-7.25). These findings suggest that breast cancer risk has a strong genetic component and supports the theory that the underlying mechanism of "complex traits" can be understood using a multigenic model of candidate genes.

Published
2001

3. Trans-ethnic analysis of metabochip data identifies two new loci associated with BMI

Author

Gong, J, primary, Nishimura, K K, additional, Fernandez-Rhodes, L, additional, Haessler, J, additional, Bien, S, additional, Graff, M, additional, Lim, U, additional, Lu, Y, additional, Gross, M, additional, Fornage, M, additional, Yoneyama, S, additional, Isasi, C R, additional, Buzkova, P, additional, Daviglus, M, additional, Lin, D-Y, additional, Tao, R, additional, Goodloe, R, additional, Bush, W S, additional, Farber-Eger, E, additional, Boston, J, additional, Dilks, H H, additional, Ehret, G, additional, Gu, C C, additional, Lewis, C E, additional, Nguyen, K-D H, additional, Cooper, R, additional, Leppert, M, additional, Irvin, M R, additional, Bottinger, E P, additional, Wilkens, L R, additional, Haiman, C A, additional, Park, L, additional, Monroe, K R, additional, Cheng, I, additional, Stram, D O, additional, Carlson, C S, additional, Jackson, R, additional, Kuller, L, additional, Houston, D, additional, Kooperberg, C, additional, Buyske, S, additional, Hindorff, L A, additional, Crawford, D C, additional, Loos, R J F, additional, Le Marchand, L, additional, Matise, T C, additional, North, K E, additional, and Peters, U, additional

Published
2017
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4. Gene-environment interactions in cancer epidemiology: A national cancer institute think tank report

Author

Hutter, C. M., Mechanic, L. E., Chatterjee, N., Kraft, P., Gillanders, E. M., Abnet, C. C., Amos, C., Balshaw, D., Bickeböller, H., Bierut, L. J., Boffetta, P., Bondy, M., Chanock, S., Chen, H. -S., Cox, N., Vivo, I. D., Divi, R., Dupuis, J., Ellison, G., Fallin, M. D., Gauderman, W. J., Gillanders, E., Haiman, C., Hutter, C., Simonds, N. I., Iversen, E., Khoury, M. J., Marchand, L. L., McAllister, K., Mechanic, L., Peters, U., Prentice, R., Rebbeck, T., Reedy, J., Rothman, N., Schully, S., Seminara, D., Shaughnessy, D., Shete, S., Spiegelman, D., Stram, D. O., BALDWIN, THOMAS DONALD, Wang, M., WANG, WENPING, WEINBERG, CAREN HELENE, Winn, D. M., Witte, J. S., Hutter, C.M., Mechanic, L.E., Chatterjee, N., Kraft, P., Gillanders, E.M., Abnet, C.C., Amos, C., Balshaw, D., Bickeböller, H., Bierut, L.J., Boffetta, P., Bondy, M., Chanock, S., Chen, H.-S., Cox, N., Vivo, I.D., Divi, R., Dupuis, J., Ellison, G., Fallin, M.D., Gauderman, W.J., Gillanders, E., Haiman, C., Hutter, C., Simonds, N.I., Iversen, E., Khoury, M.J., Marchand, L.L., McAllister, K., Mechanic, L., Peters, U., Prentice, R., Rebbeck, T., Reedy, J., Rothman, N., Schully, S., Seminara, D., Shaughnessy, D., Shete, S., Spiegelman, D., Stram, D.O., Thomas, D., Wang, M., Wang, W., Weinberg, C., Winn, D.M., and Witte, J.S.

Subjects
Gene-environment interactions, complex phenotypes, genetic epidemiology
Abstract

Cancer risk is determined by a complex interplay of genetic and environmental factors. Genome-wide association studies (GWAS) have identified hundreds of common (minor allele frequency [MAF] > 0.05) and less common (0.01 < MAF < 0.05) genetic variants associated with cancer. The marginal effects of most of these variants have been small (odds ratios: 1.1-1.4). There remain unanswered questions on how best to incorporate the joint effects of genes and environment, including gene-environment (G × E) interactions, into epidemiologic studies of cancer. To help address these questions, and to better inform research priorities and allocation of resources, the National Cancer Institute sponsored a "Gene-Environment Think Tank" on January 10-11, 2012. The objective of the Think Tank was to facilitate discussions on (1) the state of the science, (2) the goals of G × E interaction studies in cancer epidemiology, and (3) opportunities for developing novel study designs and analysis tools. This report summarizes the Think Tank discussion, with a focus on contemporary approaches to the analysis of G × E interactions. Selecting the appropriate methods requires first identifying the relevant scientific question and rationale, with an important distinction made between analyses aiming to characterize the joint effects of putative or established genetic and environmental factors and analyses aiming to discover novel risk factors or novel interaction effects. Other discussion items include measurement error, statistical power, significance, and replication. Additional designs, exposure assessments, and analytical approaches need to be considered as we move from the current small number of success stories to a fuller understanding of the interplay of genetic and environmental factors. © 2013 WILEY PERIODICALS, INC.

Published
2013

5. CYP17 Genetic Variation and Risk of Breast and Prostate Cancer from the National Cancer Institute Breast and Prostate Cancer Cohort Consortium (BPC3)

Author

Setiawan, V W, Schumacher, F R, Haiman, C A, Stram, D O, Albanes, D, Altshuler, D, Berglund, G, Buring, J, Calle, E E, Clavel-Chapelon, F, Cox, D G, Gaziano, J M, Hankinson, S E, Hayes, R B, Henderson, B E, Hirschhorn, J N, Hoover, R, Hunter, D J, Kaaks, R, Kolonel, L N, Kraft, P, Ma, J, LeMarchand, L, Linseisen, J, Lund, E, Navarro, C, Overvad, Kim, Palli, D, Peeters, P H, Pike, M C, Riboli, E, Stampfer, M J, Thun, M J, Travis, R C, Trichopoulos, D, Yeager, M, Ziegler, R G, Feigelson, H S, and Chanock, S J

Published
2007

7. 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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8. Trans-ethnic analysis of metabochip data identifies two new loci associated with BMI

Author

Gong, J, Nishimura, K K, Fernandez-Rhodes, L, Haessler, J, Bien, S, Graff, M, Lim, U, Lu, Y, Gross, M, Fornage, M, Yoneyama, S, Isasi, C R, Buzkova, P, Daviglus, M, Lin, D-Y, Tao, R, Goodloe, R, Bush, W S, Farber-Eger, E, Boston, J, Dilks, H H, Ehret, G, Gu, C C, Lewis, C E, Nguyen, K-D H, Cooper, R, Leppert, M, Irvin, M R, Bottinger, E P, Wilkens, L R, Haiman, C A, Park, L, Monroe, K R, Cheng, I, Stram, D O, Carlson, C S, Jackson, R, Kuller, L, Houston, D, Kooperberg, C, Buyske, S, Hindorff, L A, Crawford, D C, Loos, R J F, Le Marchand, L, Matise, T C, North, K E, and Peters, U

Abstract

Objective:Body mass index (BMI) is commonly used to assess obesity, which is associated with numerous diseases and negative health outcomes. BMI has been shown to be a heritable, polygenic trait, with close to 100 loci previously identified and replicated in multiple populations. We aim to replicate known BMI loci and identify novel associations in a trans-ethnic study population.Subjects:Using eligible participants from the Population Architecture using Genomics and Epidemiology consortium, we conducted a trans-ethnic meta-analysis of 102?514 African Americans, Hispanics, Asian/Native Hawaiian, Native Americans and European Americans. Participants were genotyped on over 200?000 SNPs on the Illumina Metabochip custom array, or imputed into the 1000 Genomes Project (Phase I). Linear regression of the natural log of BMI, adjusting for age, sex, study site (if applicable), and ancestry principal components, was conducted for each race/ethnicity within each study cohort. Race/ethnicity-specific, and combined meta-analyses used fixed-effects models.Results:We replicated 15 of 21 BMI loci included on the Metabochip, and identified two novel BMI loci at 1q41 (rs2820436) and 2q31.1 (rs10930502) at the Metabochip-wide significance threshold (P<2.5 × 10-7). Bioinformatic functional investigation of SNPs at these loci suggests a possible impact on pathways that regulate metabolism and adipose tissue.Conclusion:Conducting studies in genetically diverse populations continues to be a valuable strategy for replicating known loci and uncovering novel BMI associations.

Published
2018
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9. Segregation analysis of continuous phenotypes by using higher sample moments

Author

Lee, H. and Stram, D. O.

Subjects
Male, Models, Statistical, Models, Genetic, Genetic Variation, Nuclear Family, Pedigree, Genetics, Population, Phenotype, Humans, Computer Simulation, Female, Mathematics, Software, Research Article, Probability
Abstract

The present article discusses the use of computational methods based on generalized estimating equations (GEE), as a potential alternative to full maximum-likelihood methods, for performing segregation analysis of continuous phenotypes by using randomly selected family data. The method that we propose can estimate effect and degree of dominance of a major gene in the presence of additional nongenetic or polygenetic familial associations, by relating sample moments to their expectations calculated under the genetic model. It is known that all parameters in basic major-gene models cannot be identified, for estimation purposes, solely in terms of the first two sample moments of data from randomly selected families. Thus, we propose the use of higher (third order) sample moments to resolve this identifiability problem, in a pseudo-profile likelihood estimation scheme. In principle, our methods may be applied to fitting genetic models by using complex pedigrees and for estimation in the presence of missing phenotype data for family members. In order to assess its statistical efficiency we compare several variants of the method with each other and with maximum-likelihood estimates provided by the SAGE computer package in a simulation study.

Published
1996

10. Association of Type 2 Diabetes Susceptibility Variants With Advanced Prostate Cancer Risk in the Breast and Prostate Cancer Cohort Consortium

Author

Machiela, M. J., primary, Lindstrom, S., additional, Allen, N. E., additional, Haiman, C. A., additional, Albanes, D., additional, Barricarte, A., additional, Berndt, S. I., additional, Bueno-de-Mesquita, H. B., additional, Chanock, S., additional, Gaziano, J. M., additional, Gapstur, S. M., additional, Giovannucci, E., additional, Henderson, B. E., additional, Jacobs, E. J., additional, Kolonel, L. N., additional, Krogh, V., additional, Ma, J., additional, Stampfer, M. J., additional, Stevens, V. L., additional, Stram, D. O., additional, Tjonneland, A., additional, Travis, R., additional, Willett, W. C., additional, Hunter, D. J., additional, Le Marchand, L., additional, and Kraft, P., additional

Published
2012
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12. Interactions Between Genetic Variants and Breast Cancer Risk Factors in the Breast and Prostate Cancer Cohort Consortium

Author

Campa, D., primary, Kaaks, R., additional, Le Marchand, L., additional, Haiman, C. A., additional, Travis, R. C., additional, Berg, C. D., additional, Buring, J. E., additional, Chanock, S. J., additional, Diver, W. R., additional, Dostal, L., additional, Fournier, A., additional, Hankinson, S. E., additional, Henderson, B. E., additional, Hoover, R. N., additional, Isaacs, C., additional, Johansson, M., additional, Kolonel, L. N., additional, Kraft, P., additional, Lee, I.-M., additional, McCarty, C. A., additional, Overvad, K., additional, Panico, S., additional, Peeters, P. H. M., additional, Riboli, E., additional, Sanchez, M. J., additional, Schumacher, F. R., additional, Skeie, G., additional, Stram, D. O., additional, Thun, M. J., additional, Trichopoulos, D., additional, Zhang, S., additional, Ziegler, R. G., additional, Hunter, D. J., additional, Lindstrom, S., additional, and Canzian, F., additional

Published
2011
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13. Type 2 diabetes risk variants and colorectal cancer risk: the Multiethnic Cohort and PAGE studies

Author

Cheng, I., primary, Caberto, C. P., additional, Lum-Jones, A., additional, Seifried, A., additional, Wilkens, L. R., additional, Schumacher, F. R., additional, Monroe, K. R., additional, Lim, U., additional, Tiirikainen, M., additional, Kolonel, L. N., additional, Henderson, B. E., additional, Stram, D. O., additional, Haiman, C. A., additional, and Le Marchand, L., additional

Published
2011
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19. Diet and Risk of Ovarian Cancer in the California Teachers Study Cohort

Author

Chang, E. T., primary, Lee, V. S., additional, Canchola, A. J., additional, Clarke, C. A., additional, Purdie, D. M., additional, Reynolds, P., additional, Anton-Culver, H., additional, Bernstein, L., additional, Deapen, D., additional, Peel, D., additional, Pinder, R., additional, Ross, R. K., additional, Stram, D. O., additional, West, D. W., additional, Wright, W., additional, Ziogas, A., additional, and Horn-Ross, P. L., additional

Published
2007
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36. Genetic predisposition to radiation-related cancer and potential implications for risk assessment.

Author

Sigurdson, A J and Stram, D O

Abstract

Several lines of evidence suggest that risk estimates for cancer associated with radiation exposure incorporate individuals who are more and less inherently susceptible to the carcinogenic effects of radiation, and the technology to further evaluate this issue is now available. For example, genome-wide association scan studies could be undertaken to address, at least in part, the direction of causality in the observations of differential sensitivity to radiomimetic agents in cancer cases compared with normal individuals, thereby building on previous observations that sensitivity to these agents is higher in apparently normal individuals carrying gene mutations in NBS and ATM. Direct studies of risk of second cancers in relation to radiation are underway, and some results have been reported (e.g. for the PRDM1 gene as related to sensitivity to radiation-related cancers after treatment for Hodgkin's lymphoma). It is important to understand the risk synergies between variants affecting associations with various cancers defining susceptibility in unexposed populations and the excess risk in populations therapeutically or occupationally exposed to radiation for the purpose of risk protection, especially as additional baseline risk variants are discovered in increasingly large-scale analyses. While there are studies that are beginning to address these questions, there have been no compelling new discoveries, to date, to indicate that predisposition information should be included in risk assessment. The conclusions in ICRP Publications 79 and 103 appear relevant today. [ABSTRACT FROM AUTHOR]

Published
2012
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37. A candidate gene approach to searching for low-penetrance breast and prostate cancer genes.

Author

Hunter, D J, Riboli, E, Haiman, C A, Albanes, D, Altshuler, D, Chanock, S J, Haynes, R B, Henderson, B E, Kaaks, R, Stram, D O, Thomas, G, Thun, M J, Blanché, H, Buring, J E, Burtt, N P, Calle, E E, Cann, H, Canzian, F, Chen, Y C, and Colditz, G A

Subjects
BREAST tumors, SEX hormones, LONGITUDINAL method, ONCOGENES, PROSTATE tumors, PHENOTYPES
Abstract

Most cases of breast and prostate cancer are not associated with mutations in known high-penetrance genes, indicating the involvement of multiple low-penetrance risk alleles. Studies that have attempted to identify these genes have met with limited success. The National Cancer Institute Breast and Prostate Cancer Cohort Consortium--a pooled analysis of multiple large cohort studies with a total of more than 5,000 cases of breast cancer and 8,000 cases of prostate cancer--was therefore initiated. The goal of this consortium is to characterize variations in approximately 50 genes that mediate two pathways that are associated with these cancers--the steroid-hormone metabolism pathway and the insulin-like growth factor signalling pathway--and to associate these variations with cancer risk. [ABSTRACT FROM AUTHOR]

Published
2005
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38. Histopathology (International Neuroblastoma Pathology Classification) and MYCN status in patients with peripheral neuroblastic tumors: a report from the Children's Cancer Group.

Author

Goto, Shoko, Umehara, Shunsuke, Gerbing, Robert B., Stram, Daniel O., Brodeur, Garrett M., Seeger, Robert C., Lukens, John N., Matthay, Katherine K., Shimada, Hiroyuki, Goto, S, Umehara, S, Gerbing, R B, Stram, D O, Brodeur, G M, Seeger, R C, Lukens, J N, Matthay, K K, and Shimada, H

Published
2001
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39. International neuroblastoma pathology classification for prognostic evaluation of patients with peripheral neuroblastic tumors: a report from the Children's Cancer Group.

Author

Shimada, Hiroyuki, Umehara, Shunsuke, Monobe, Yasumasa, Hachitanda, Yoichi, Nakagawa, Atsuko, Goto, Shoko, Gerbing, Robert B., Stram, Daniel O., Lukens, John N., Matthay, Katherine K., Shimada, H, Umehara, S, Monobe, Y, Hachitanda, Y, Nakagawa, A, Goto, S, Gerbing, R B, Stram, D O, Lukens, J N, and Matthay, K K

Published
2001
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40. Genome-Wide Meta-Analyses of Breast, Ovarian, and Prostate Cancer Association Studies Identify Multiple New Susceptibility Loci Shared by at Least Two Cancer Types

Author

Kar, S. P., Beesley, J., Amin Al Olama, A., Michailidou, K., Tyrer, J., Kote-Jarai, Z., Lawrenson, K., Lindstrom, S., Ramus, S. J., Thompson, D. J., Kibel, Adam Stuart, Dansonka-Mieszkowska, A., Michael, A., Dieffenbach, A. K., Gentry-Maharaj, A., Whittemore, A. S., Wolk, A., Monteiro, A., Peixoto, A., Kierzek, A., Cox, A., Rudolph, A., Gonzalez-Neira, A., Wu, A. H., Lindblom, A., Swerdlow, A., Ziogas, A., Ekici, A. B., Burwinkel, B., Karlan, B. Y., Nordestgaard, B. G., Blomqvist, C., Phelan, C., McLean, C., Pearce, C. L., Vachon, C., Cybulski, C., Slavov, C., Stegmaier, C., Maier, C., Ambrosone, C. B., Hogdall, C. K., Teerlink, C. C., Kang, D., Tessier, D. C., Schaid, D. J., Stram, D. O., Cramer, Daniel William, Neal, D. E., Eccles, D., Flesch-Janys, D., Edwards, D. R. V., Wokozorczyk, D., Levine, D. A., Yannoukakos, D., Sawyer, E. J., Bandera, E. V., Poole, Elizabeth M., Goode, E. L., Khusnutdinova, E., Hogdall, E., Song, F, Bruinsma, F., Heitz, F., Modugno, F., Hamdy, F. C., Wiklund, F., Giles, G. G., Olsson, H., Wildiers, H., Ulmer, H.-U., Pandha, H., Risch, H. A., Darabi, H., Salvesen, H. B., Nevanlinna, H., Gronberg, H., Brenner, H., Brauch, H., Anton-Culver, H., Song, H., Lim, H.-Y., McNeish, I., Campbell, I., Vergote, I., Gronwald, J., Lubinski, J., Stanford, J. L., Benitez, J., Doherty, J. A., Permuth, J. B., Chang-Claude, J., Donovan, J. L., Dennis, J., Schildkraut, J. M., Schleutker, J., Hopper, J. L., Kupryjanczyk, J., Park, J. Y., Figueroa, J., Clements, J. A., Knight, J. A., Peto, J., Cunningham, J. M., Pow-Sang, J., Batra, J., Czene, K., Lu, K. H., Herkommer, K., Khaw, K.-T., Matsuo, K., Muir, K., Offitt, K., Chen, K., Moysich, K. B., Aittoma ki, K., Odunsi, K., Kiemeney, L. A., Massuger, L. F. A. G., Fitzgerald, L. M., Cook, L. S., Cannon-Albright, L., Hooning, M. J., Pike, M. C., Bolla, M. K., Luedeke, M., Teixeira, M. R., Goodman, M. T., Schmidt, M. K., Riggan, M., Aly, M., Rossing, M. A., Beckmann, M. W., Moisse, M., Sanderson, M., Southey, M. C., Jones, M., Lush, M., Hildebrandt, M. A. T., Hou, M.-F., Schoemaker, M. J., Garcia-Closas, M., Bogdanova, N., Rahman, N., Le, N. D., Orr, N., Wentzensen, N., Pashayan, N., Peterlongo, P., Guenel, P., Brennan, P., Paulo, P., Webb, P. M., Broberg, P., Fasching, P. A., Devilee, P., Wang, Q., Cai, Q., Li, Q., Kaneva, R., Butzow, R., Kopperud, R. K., Schmutzler, R. K., Stephenson, R. A., MacInnis, R. J., Hoover, R. N., Winqvist, R., Ness, R., Milne, R. L., Travis, R. C., Benlloch, S., Olson, S. H., McDonnell, S. K., Tworoger, Shelley Slate, Maia, S., Berndt, S., Lee, S. C., Teo, S.-H., Thibodeau, S. N., Bojesen, S. E., Gapstur, S. M., Kjaer, S. K., Pejovic, T., Tammela, T. L. J., Do rk, T., Bru ning, T., Wahlfors, T., Key, T. J., Edwards, T. L., Menon, U., Hamann, U., Mitev, V., Kosma, V.-M., Setiawan, V. W., Kristensen, V., Arndt, V., Vogel, W., Zheng, W., Sieh, W., Blot, W. J., Kluzniak, W., Shu, X.-O., Gao, Y.-T., Schumacher, F., Freedman, M. L., Berchuck, A., Dunning, A. M., Simard, J., Haiman, C. A., Spurdle, A., Sellers, T. A., Hunter, David J., Henderson, B. E., Kraft, Peter Elias, Chanock, S. J., Couch, F. J., Hall, P., Gayther, S. A., Easton, D. F., Chenevix-Trench, G., Eeles, R., Pharoah, P. D. P., Lambrechts, D., and undefined, undefined

Subjects
breast cancer, ovarian cancer, prostate cancer, genome-wide association studies, pleiotropy
Abstract

Breast, ovarian, and prostate cancers are hormone-related and may have a shared genetic basis, but this has not been investigated systematically by genome-wide association (GWA) studies. Meta-analyses combining the largest GWA meta-analysis data sets for these cancers totaling 112,349 cases and 116,421 controls of European ancestry, all together and in pairs, identified at P < 10(-8) seven new cross-cancer loci: three associated with susceptibility to all three cancers (rs17041869/2q13/BCL2L11; rs7937840/11q12/INCENP; rs1469713/19p13/GATAD2A), two breast and ovarian cancer risk loci (rs200182588/9q31/SMC2; rs8037137/15q26/RCCD1), and two breast and prostate cancer risk loci (rs5013329/1p34/NSUN4; rs9375701/6q23/L3MBTL3). Index variants in five additional regions previously associated with only one cancer also showed clear association with a second cancer type. Cell-type-specific expression quantitative trait locus and enhancer-gene interaction annotations suggested target genes with potential cross-cancer roles at the new loci. Pathway analysis revealed significant enrichment of death receptor signaling genes near loci with P < 10(-5) in the three-cancer meta-analysis., Other Research Unit

Published
2016
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41. Genome-wide Analysis Identifies Novel Loci Associated with Ovarian Cancer Outcomes: Findings from the Ovarian Cancer Association Consortium

Author

Johnatty, S. E., Tyrer, J. P., Kar, S., Beesley, J., Lu, Y., Gao, B., Fasching, P. A., Hein, A., Ekici, A. B., Beckmann, M. W., Lambrechts, D., Van Nieuwenhuysen, E., Vergote, I., Lambrechts, S., Rossing, M. A., Doherty, J. A., Chang-Claude, J., Modugno, F., Ness, R. B., Moysich, K. B., Levine, D. A., Kiemeney, L. A., Massuger, L. F. A. G., Gronwald, J., Lubinski, J., Jakubowska, A., Cybulski, C., Brinton, L., Lissowska, J., Wentzensen, N., Song, H., Rhenius, V., Campbell, I., Eccles, D., Sieh, W., Whittemore, A. S., McGuire, V., Rothstein, J. H., Sutphen, R., Anton-Culver, H., Ziogas, A., Gayther, S. A., Gentry-Maharaj, A., Menon, U., Ramus, S. J., Pearce, C. L., Pike, M. C., Stram, D. O., Wu, A. H., Kupryjanczyk, J., Dansonka-Mieszkowska, A., Rzepecka, I. K., Spiewankiewicz, B., Goodman, M. T., Wilkens, L. R., Carney, M. E., Thompson, P. J., Heitz, F., du Bois, A., Schwaab, I., Harter, P., Pisterer, J., Hillemanns, P., Karlan, B. Y., Walsh, C., Lester, J., Orsulic, S., Winham, S. J., Earp, M., Larson, M. C., Fogarty, Z. C., Hogdall, E., Jensen, A., Kjaer, S. K., Fridley, B. L., Cunningham, J. M., Vierkant, R. A., Schildkraut, J. M., Iversen, E. S., Terry, Kathryn Lynne, Cramer, Daniel William, Bandera, E. V., Orlow, I., Pejovic, T., Bean, Y., Hogdall, C., Lundvall, L., McNeish, I., Paul, J., Carty, K., Siddiqui, N., Glasspool, R., Sellers, T., Kennedy, C., Chiew, Y.-E., Berchuck, A., MacGregor, S., Pharoah, P. D. P., Goode, E. L., deFazio, A., Webb, P. M., and Chenevix-Trench, G.

Subjects
progression-free survival, overall survival, epithelial ovarian cancer, lncRNA, chemotherapy
Abstract

PURPOSE: Chemotherapy resistance remains a major challenge in the treatment of ovarian cancer. We hypothesize that germline polymorphisms might be associated with clinical outcome. EXPERIMENTAL DESIGN: We analyzed approximately 2.8 million genotyped and imputed SNPs from the iCOGS experiment for progression-free survival (PFS) and overall survival (OS) in 2,901 European epithelial ovarian cancer (EOC) patients who underwent first-line treatment of cytoreductive surgery and chemotherapy regardless of regimen, and in a subset of 1,098 patients treated with ≥ 4 cycles of paclitaxel and carboplatin at standard doses. We evaluated the top SNPs in 4,434 EOC patients, including patients from The Cancer Genome Atlas. In addition, we conducted pathway analysis of all intragenic SNPs and tested their association with PFS and OS using gene set enrichment analysis. RESULTS: Five SNPs were significantly associated (P ≤ 1.0 × 10(-5)) with poorer outcomes in at least one of the four analyses, three of which, rs4910232 (11p15.3), rs2549714 (16q23), and rs6674079 (1q22), were located in long noncoding RNAs (lncRNAs) RP11-179A10.1, RP11-314O13.1, and RP11-284F21.8, respectively (P ≤ 7.1 × 10(-6)). ENCODE ChIP-seq data at 1q22 for normal ovary show evidence of histone modification around RP11-284F21.8, and rs6674079 is perfectly correlated with another SNP within the super-enhancer MEF2D, expression levels of which were reportedly associated with prognosis in another solid tumor. YAP1- and WWTR1 (TAZ)-stimulated gene expression and high-density lipoprotein (HDL)-mediated lipid transport pathways were associated with PFS and OS, respectively, in the cohort who had standard chemotherapy (pGSEA ≤ 6 × 10(-3)). CONCLUSIONS: We have identified SNPs in three lncRNAs that might be important targets for novel EOC therapies., Other Research Unit

Published
2015
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43. Neuroblastoma and parental occupation.

Author

Olshan, Andrew, De Roos, Anneclaire, Teschke, Kay, Neglia, Joseph, Stram, Daniel, Pollock, Brad, Castleberry, Robert, Olshan, A F, De Roos, A J, Teschke, K, Neglia, J P, Stram, D O, Pollock, B H, and Castleberry, R P

Abstract

Objectives: We evaluated parental occupation and the risk of neuroblastoma using data from a large case-control study conducted by the Children's Cancer Group and the Pediatric Oncology Group.Methods: We compared the distribution of 73 paternal and 57 maternal occupational groups among 504 newly diagnosed cases of neuroblastoma and individually matched controls obtained by telephone random digit dialing in the United States and Canada.Results: An increased risk of neuroblastoma was found for fathers employed as broadcast, telephone and dispatch operators (odds ratio [OR] = 6.1; 95% confidence interval [CI] = 0.7-50.9), electrical power installers and power plant operators (OR = 2.7; CI = 0.9-8.1), landscapers and groundskeepers (OR = 2.3; CI = 1.0-5.2), and painters (OR = 2.1; CI = 0.9-4.8). Elevated odds ratios were found for mothers employed as farmers and farm workers (OR = 2.2; CI = 0.6-8.8), florists and garden store workers (OR = 2.4; CI = 0.6-9.9), hairdressers and barbers (OR = 2.8; CI = 1.2-6.3), electric power installers and power plant operators, and sailors, fishers, and railroad workers. No increase in risk was found for other paternal occupations previously associated, including electricians, electrical equipment assemblers and repairers (OR = 1.1; CI = 0.6-2.0), or welders (OR = 0.5; CI = 0.1-1.6).Conclusion: The study reinforced some prior evidence of increased risks in electrical, farming and gardening, and painting occupations, but failed to confirm other previously reported associations. Further analyses of exposure to electromagnetic fields, metals, solvents, and pesticides are currently under way. [ABSTRACT FROM AUTHOR]

Published
1999
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48. The Role of KRAS rs61764370 in Invasive Epithelial Ovarian Cancer: Implications for Clinical Testing

Author

Pharoah, P. D. P., Palmieri, R. T., Ramus, S. J., Gayther, S. A., Andrulis, I. L., Anton-Culver, H., Antonenkova, N., Antoniou, A. C., Goldgar, D., Beattie, M. S., Beckmann, M. W., Birrer, Michael James, Bogdanova, N., Bolton, K. L., Brewster, W., Brooks-Wilson, A., Brown, R., Butzow, R., Caldes, T., Caligo, M. A., Campbell, I., Chang-Claude, J., Chen, Y. A., Cook, L. S., Couch, F. J., Cramer, Daniel William, Cunningham, J. M., Despierre, E., Doherty, J. A., Dork, T., Durst, M., Eccles, D. M., Ekici, A. B., Easton, D., Fasching, P. A., de Fazio, A., Fenstermacher, D. A., Flanagan, J. M., Fridley, B. L., Friedman, E., Gao, B., Sinilnikova, O., Gentry-Maharaj, A., Godwin, A. K., Goode, E. L., Goodman, M. T., Gross, J., Hansen, T. V. O., Harnett, P., Rookus, M., Heikkinen, T., Hein, R., Hogdall, C., Hogdall, E., Iversen, E. S., Jakubowska, A., Johnatty, S. E., Karlan, B. Y., Kauff, N. D., Kaye, S. B., Chenevix-Trench, G., Kelemen, L. E., Kiemeney, L. A., Kjaer, S. K., Lambrechts, D., LaPolla, J. P., Lazaro, C., Le, N. D., Leminen, A., Leunen, K., Levine, D. A., Lu, Y., Lundvall, L., Macgregor, S., Marees, T., Massuger, L. F., McLaughlin, J. R., Menon, U., Montagna, M., Moysich, K. B., Narod, S. A., Nathanson, K. L., Nedergaard, L., Ness, R. B., Nevanlinna, H., Nickels, S., Osorio, A., Paul, J., Pearce, C. L., Phelan, C. M., Pike, M. C., Radice, P., Rossing, M. A., Schildkraut, J. M., Sellers, T. A., Singer, C. F., Song, H., Stram, D. O., Sutphen, R., Lindblom, A., Terry, Kathryn Lynne, Tsai, Y.-Y., van Altena, A. M., Vergote, I., Vierkant, R. A., Vitonis, A. F., Walsh, C., Wang-Gohrke, S., Wappenschmidt, B., Wu, A. H., Ziogas, A., Berchuck, A., and Risch, H. A.

Abstract

Purpose An assay for the single nucleotide polymorphism (SNP) rs61764370 has recently been commercially marketed as a clinical test to aid ovarian cancer risk evaluation in women with family histories of the disease. rs67164370 is in a 3′UTR miRNA binding site of the KRAS oncogene, and is a candidate for epithelial ovarian cancer (EOC) susceptibility. However, only one published paper, analyzing fewer than 1,000 subjects in total, has examined this association. Experimental Design Risk association was evaluated in 8,669 cases of invasive EOC and 10,012 controls from nineteen studies participating in the Ovarian Cancer Association Consortium, and in 683 cases and 2,044 controls carrying BRCA1 mutations from studies in the Consortium of Investigators of Modifiers of BRCA1/2. Prognosis association was also examined in a subset of five studies with progression-free survival data and eighteen studies with all-cause mortality data. Results No evidence of association was observed between genotype and risk of unselected EOC (odds ratio (OR)=1.02, 95% confidence interval (CI)=0.95–1.10), serous EOC (OR=1.08, 95%CI=0.98–1.18), familial EOC (OR=1.09, 95%CI=0.78–1.54), or among women carrying deleterious mutations in BRCA1 (OR=1.09, 95%CI=0.88–1.36). There was little evidence for association with survival time among unselected cases (hazard ratio (HR)=1.10, 95%CI=0.99–1.22), among serous cases (HR=1.12, 95%CI=0.99–1.28), or with progression-free survival in 540 cases treated with carboplatin and paclitaxel (HR=1.18, 95%CI=0.93–1.52). Conclusions These data exclude the possibility of an association between rs61764370 and a clinically significant risk of ovarian cancer or of familial ovarian cancer. Use of this SNP for ovarian cancer clinical risk prediction therefore appears unwarranted.

Published
2011
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49. Prostate Cancer Susceptibility Polymorphism rs2660753 Is Not Associated with Invasive Ovarian Cancer

Author

Amankwah, E. K., Kelemen, L. E., Wang, Q., Song, H., Chenevix-Trench, G., Beesley, J., Webb, P. M., Pearce, C. L., Wu, A. H., Pike, M. C., Stram, D. O., Chang-Claude, J., Wang-Gohrke, S., Ness, R. B., Goode, E. L., Cunningham, J. M., Fridley, B. L., Vierkant, R. A., Tworoger, Shelley Slate, Whittemore, A. S., McGuire, V., Sieh, W., Gayther, S. A., Gentry-Maharaj, A., Menon, U., Ramus, S. J., Rossing, M. A., Doherty, J. A., Goodman, M. T., Carney, M. E., Lurie, G., Wilkens, L. R., Kruger Kjaer, S., Hogdall, E., Cramer, Daniel William, Terry, Kathryn Lynne, Garcia-Closas, M., Yang, H., Lissowska, J., Anton-Culver, H., Ziogas, A., Schildkraut, J. M., Berchuck, A., and Pharoah, P. D. P.

Subjects
chromosome 3p, SNP, ovarian cancer, risk factors
Abstract

Background We previously reported an association between rs2660753, a prostate cancer susceptibility polymorphism, and invasive epithelial ovarian cancer (EOC) [odds ratio (OR)=1.2, 95% confidence interval (CI)=1.0-1.4, Ptrend=0.01] that showed a stronger association with the serous histological subtype (OR=1.3, 95% CI=1.1-1.5, Ptrend=0.003). Methods We sought to replicate this association in 12 other studies comprising 4,482 cases and 6,894 controls of white non-Hispanic ancestry in the Ovarian Cancer Association Consortium. Results No evidence for an association with all cancers or serous cancers was observed in a combined analysis of data from the replication studies (all: OR=1.0, 95% CI=0.9-1.1, Ptrend=0.61; serous: OR=1.0, 95% CI=0.9-1.1, Ptrend=0.85) or from the combined analysis of discovery and replication studies (all: OR=1.0, 95% CI=1.0-1.1, Ptrend= 0.28; serous: OR=1.1, 95% CI=1.0-1.2, Ptrend=0.11). There was no evidence for statistical heterogeneity in ORs across the studies. Conclusions Although rs2660753 is a strong a prostate cancer susceptibility polymorphism, the association with another hormonally related cancer, invasive EOC, is not supported by this replication study. Impact Our findings, based on a larger sample size, emphasize the importance of replicating potentially promising genetic risk associations.

Published
2011
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50. Genetic Variation in TYMS in the One-Carbon Transfer Pathway Is Associated with Ovarian Carcinoma Types in the Ovarian Cancer Association Consortium

Author

Kelemen, L. E., Goodman, M. T., McGuire, V., Rossing, M. A., Webb, P. M., Kobel, M., Anton-Culver, H., Beesley, J., Berchuck, A., Brar, S., Carney, M. E., Chang-Claude, J., Chenevix-Trench, G., Cramer, Daniel William, Cunningham, J. M., DiCioccio, R. A., Doherty, J. A., Easton, D. F., Fredericksen, Z. S., Fridley, B. L., Gates, M. A., Gayther, S. A., Gentry-Maharaj, A., Hogdall, E., Kjaer, S. K., Lurie, G., Menon, U., Moorman, P. G., Moysich, K., Ness, R. B., Palmieri, R. T., Pearce, C. L., Pharoah, P. D. P., Ramus, S. J., Song, H., Stram, D. O., Tworoger, Shelley Slate, Van Den Berg, D., Vierkant, R. A., Wang-Gohrke, S., Whittemore, A. S., Wilkens, L. R., Wu, A. H., Schildkraut, J. M., Sellers, T. A., and Goode, E. L.

Abstract

Background We previously reported risks of ovarian carcinoma for common polymorphisms in one-carbon (1-C) transfer genes. We sought to replicate associations for DPYD rs1801265, DNMT3A rs13420827, MTHFD1 rs1950902, MTHFS rs17284990 and TYMS rs495139 with risk of ovarian carcinoma overall, and to utilize the large sample of assembled cases to investigate associations by histological type. Methods Associations were evaluated in the Ovarian Cancer Association Consortium, including 16 studies of 5,593 epithelial ovarian carcinoma cases and 9,962 controls of white non-Hispanic origin. Odds ratios (OR) and 95% confidence intervals (CI) were adjusted for age and study site. Results The five polymorphisms were not associated with ovarian carcinoma overall (P trend > 0.13); however, associations for the minor allele at TYMS rs495139 were observed for carcinomas of mucinous type (OR, 1.19; 95% CI, 1.03-1.39; P = 0.02), clear cell type (OR, 0.86; 95% CI, 0.75-0.99; P = 0.04) and endometrioid type (OR, 0.90; 95% CI, 0.81-0.99; P = 0.04) (P heterogeneity = 0.001). Restriction to low-grade mucinous carcinomas further strengthened the association for the mucinous type (OR, 1.32; 95% CI, 1.07-1.62; P = 0.01). TYMS rs495139 was not associated with serous type (OR, 1.06; 95% CI, 1.00-1.13; P = 0.05). Conclusions TYMS rs495139 may be associated with a differential risk of ovarian carcinoma types, indicating the importance of accurate histopathological classification. Impact Biomarkers that distinguish ovarian carcinoma types are few, and TYMS rs495139 may provide a novel clue to type etiology. Additional genotyping in a larger sample with increased gene coverage is underway.

Published
2010
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