Person:
Ma, Jing

Profile Picture

Email Address

AA Acceptance Date

Birth Date

Research Projects

Organizational Units

Job Title

Last Name

Ma

First Name

Jing

Name

Ma, Jing
Author's Publications: search.filters.isAuthorOfPublication.d0677a65-2b21-4126-b2a9-683da6c299a9

Search Results

Now showing 1 - 10 of 11
  • Thumbnail Image
    Publication
    Fine-mapping of prostate cancer susceptibility loci in a large meta-analysis identifies candidate causal variants
    (Nature Publishing Group UK, 2018) Dadaev, Tokhir; Saunders, Edward J.; Newcombe, Paul J.; Anokian, Ezequiel; Leongamornlert, Daniel A.; Brook, Mark N.; Cieza-Borrella, Clara; Mijuskovic, Martina; Wakerell, Sarah; Olama, Ali Amin Al; Schumacher, Fredrick R.; Berndt, Sonja I.; Benlloch, Sara; Ahmed, Mahbubl; Goh, Chee; Sheng, Xin; Zhang, Zhuo; Muir, Kenneth; Govindasami, Koveela; Lophatananon, Artitaya; Stevens, Victoria L.; Gapstur, Susan M.; Carter, Brian D.; Tangen, Catherine M.; Goodman, Phyllis; Thompson, Ian M.; Batra, Jyotsna; Chambers, Suzanne; Moya, Leire; Clements, Judith; Horvath, Lisa; Tilley, Wayne; Risbridger, Gail; Gronberg, Henrik; Aly, Markus; Nordström, Tobias; Pharoah, Paul; Pashayan, Nora; Schleutker, Johanna; Tammela, Teuvo L. J.; Sipeky, Csilla; Auvinen, Anssi; Albanes, Demetrius; Weinstein, Stephanie; Wolk, Alicja; Hakansson, Niclas; West, Catharine; Dunning, Alison M.; Burnet, Neil; Mucci, Lorelei; Giovannucci, Edward; Andriole, Gerald; Cussenot, Olivier; Cancel-Tassin, Géraldine; Koutros, Stella; Freeman, Laura E. Beane; Sorensen, Karina Dalsgaard; Orntoft, Torben Falck; Borre, Michael; Maehle, Lovise; Grindedal, Eli Marie; Neal, David E.; Donovan, Jenny L.; Hamdy, Freddie C.; Martin, Richard M.; Travis, Ruth C.; Key, Tim J.; Hamilton, Robert J.; Fleshner, Neil E.; Finelli, Antonio; Ingles, Sue Ann; Stern, Mariana C.; Rosenstein, Barry; Kerns, Sarah; Ostrer, Harry; Lu, Yong-Jie; Zhang, Hong-Wei; Feng, Ninghan; Mao, Xueying; Guo, Xin; Wang, Guomin; Sun, Zan; Giles, Graham G.; Southey, Melissa C.; MacInnis, Robert J.; FitzGerald, Liesel M.; Kibel, Adam S.; Drake, Bettina F.; Vega, Ana; Gómez-Caamaño, Antonio; Fachal, Laura; Szulkin, Robert; Eklund, Martin; Kogevinas, Manolis; Llorca, Javier; Castaño-Vinyals, Gemma; Penney, Kathryn; Stampfer, Meir; Park, Jong Y.; Sellers, Thomas A.; Lin, Hui-Yi; Stanford, Janet L.; Cybulski, Cezary; Wokolorczyk, Dominika; Lubinski, Jan; Ostrander, Elaine A.; Geybels, Milan S.; Nordestgaard, Børge G.; Nielsen, Sune F.; Weisher, Maren; Bisbjerg, Rasmus; Røder, Martin Andreas; Iversen, Peter; Brenner, Hermann; Cuk, Katarina; Holleczek, Bernd; Maier, Christiane; Luedeke, Manuel; Schnoeller, Thomas; Kim, Jeri; Logothetis, Christopher J.; John, Esther M.; Teixeira, Manuel R.; Paulo, Paula; Cardoso, Marta; Neuhausen, Susan L.; Steele, Linda; Ding, Yuan Chun; De Ruyck, Kim; De Meerleer, Gert; Ost, Piet; Razack, Azad; Lim, Jasmine; Teo, Soo-Hwang; Lin, Daniel W.; Newcomb, Lisa F.; Lessel, Davor; Gamulin, Marija; Kulis, Tomislav; Kaneva, Radka; Usmani, Nawaid; Slavov, Chavdar; Mitev, Vanio; Parliament, Matthew; Singhal, Sandeep; Claessens, Frank; Joniau, Steven; Van den Broeck, Thomas; Larkin, Samantha; Townsend, Paul A.; Aukim-Hastie, Claire; Gago-Dominguez, Manuela; Castelao, Jose Esteban; Martinez, Maria Elena; Roobol, Monique J.; Jenster, Guido; van Schaik, Ron H. N.; Menegaux, Florence; Truong, Thérèse; Koudou, Yves Akoli; Xu, Jianfeng; Khaw, Kay-Tee; Cannon-Albright, Lisa; Pandha, Hardev; Michael, Agnieszka; Kierzek, Andrzej; Thibodeau, Stephen N.; McDonnell, Shannon K.; Schaid, Daniel J.; Lindstrom, Sara; Turman, Constance; Ma, Jing; Hunter, David; Riboli, Elio; Siddiq, Afshan; Canzian, Federico; Kolonel, Laurence N.; Le Marchand, Loic; Hoover, Robert N.; Machiela, Mitchell J.; Kraft, Phillip; Cook, Margaret; Thwaites, Alison; Guy, Michelle; Whitmore, Ian; Morgan, Angela; Fisher, Cyril; Hazel, Steve; Livni, Naomi; Spurdle, Amanda; Srinivasan, Srilakshmi; Kedda, Mary-Anne; Aitken, Joanne; Gardiner, Robert; Hayes, Vanessa; Butler, Lisa; Taylor, Renea; Yeadon, Trina; Eckert, Allison; Saunders, Pamela; Haynes, Anne-Maree; Papargiris, Melissa; Kujala, Paula; Talala, Kirsi; Murtola, Teemu; Taari, Kimmo; Dearnaley, David; Barnett, Gill; Bentzen, Søren; Elliott, Rebecca; Ranu, Hardeep; Hicks, Belynda; Vogt, Aurelie; Hutchinson, Amy; Cox, Angela; Davis, Michael; Brown, Paul; George, Anne; Marsden, Gemma; Lane, Athene; Lewis, Sarah J.; Berry, Clare; Kulkarni, Girish S.; Toi, Ants; Evans, Andrew; Zlotta, Alexandre R.; van der Kwast, Theodorus H.; Imai, Takashi; Saito, Shiro; Marzec, Jacek; Cao, Guangwen; Lin, Ji; Ling, Jin; Li, Meiling; Zhao, Shan-Chao; Ren, Guoping; Yu, Yongwei; Wu, Yudong; Wu, Ji; Zhou, Bo; Zhang, Yangling; Li, Jie; He, Weiyang; Guo, Jianming; Pedersen, John; Hopper, John L.; Milne, Roger; Klim, Aleksandra; Carballo, Ana; Lobato-Busto, Ramón; Peleteiro, Paula; Calvo, Patricia; Aguado, Miguel; Ruiz-Dominguez, José Manuel; Cecchini, Lluís; Mengual, Lourdes; Alcaraz, Antonio; Bustamante, Mariona; Gracia-Lavedan, Esther; Dierssen-Sotos, Trinidad; Gomez-Acebo, Ines; Pow-Sang, Julio; Park, Hyun; Zachariah, Babu; Kluzniak, Wojciech; Kolb, Suzanne; Klarskov, Peter; Stegmaier, Christa; Vogel, Walther; Herkommer, Kathleen; Bohnert, Philipp; Maia, Sofia; Silva, Maria P.; De Langhe, Sofie; Thierens, Hubert; Tan, Meng H.; Ong, Aik T.; Kastelan, Zeljko; Popov, Elenko; Kachakova, Darina; Mitkova, Atanaska; Vlahova, Aleksandrina; Dikov, Tihomir; Christova, Svetlana; Carracedo, Angel; Bangma, Christopher; Schroder, F. H.; Cenee, Sylvie; Tretarre, Brigitte; Rebillard, Xavier; Mulot, Claire; Sanchez, Marie; Adolfsson, Jan; Stattin, Par; Johansson, Jan-Erik; Cavalli-Bjoerkman, Carin; Karlsson, Ami; Broms, Michael; Wu, Huihai; Tillmans, Lori; Riska, Shaun; Freedman, Matthew; Wiklund, Fredrik; Chanock, Stephen; Henderson, Brian E.; Easton, Douglas F.; Haiman, Christopher A.; Eeles, Rosalind A.; Conti, David V.; Kote-Jarai, Zsofia
    Prostate cancer is a polygenic disease with a large heritable component. A number of common, low-penetrance prostate cancer risk loci have been identified through GWAS. Here we apply the Bayesian multivariate variable selection algorithm JAM to fine-map 84 prostate cancer susceptibility loci, using summary data from a large European ancestry meta-analysis. We observe evidence for multiple independent signals at 12 regions and 99 risk signals overall. Only 15 original GWAS tag SNPs remain among the catalogue of candidate variants identified; the remainder are replaced by more likely candidates. Biological annotation of our credible set of variants indicates significant enrichment within promoter and enhancer elements, and transcription factor-binding sites, including AR, ERG and FOXA1. In 40 regions at least one variant is colocalised with an eQTL in prostate cancer tissue. The refined set of candidate variants substantially increase the proportion of familial relative risk explained by these known susceptibility regions, which highlights the importance of fine-mapping studies and has implications for clinical risk profiling.
  • Thumbnail Image
    Publication
    Joint Effects of Colorectal Cancer Susceptibility Loci, Circulating 25-Hydroxyvitamin D and Risk of Colorectal Cancer
    (Public Library of Science, 2014) Hiraki, Linda T.; Joshi, Amit; Ng, Kimmie; Fuchs, Charles; Ma, Jing; Hazra, Aditi; Peters, Ulrike; Karlson, Elizabeth; Giovannucci, Edward; Kraft, Phillip; Chan, Andrew
    Background: Genome wide association studies (GWAS) have identified several SNPs associated with colorectal cancer (CRC) susceptibility. Vitamin D is also inversely associated with CRC risk. Methods: We examined main and joint effects of previously GWAS identified genetic markers of CRC and plasma 25-hydroxyvitamin D (25(OH)D) on CRC risk in three prospective cohorts: the Nurses' Health Study (NHS), the Health Professionals Follow-up Study (HPFS), and the Physicians' Health Study (PHS). We included 1895 CRC cases and 2806 controls with genomic DNA. We calculated odds ratios and 95% confidence intervals for CRC associated with additive genetic risk scores (GRSs) comprised of all CRC SNPs and subsets of these SNPs based on proximity to regions of increased vitamin D receptor binding to vitamin D response elements (VDREs), based on published ChiP-seq data. Among a subset of subjects with additional prediagnostic 25(OH)D we tested multiplicative interactions between plasma 25(OH)D and GRS's. We used fixed effects models to meta-analyze the three cohorts. Results: The per allele multivariate OR was 1.12 (95% CI, 1.06–1.19) for GRS-proximalVDRE; and 1.10 (95% CI, 1.06–1.14) for GRS-nonproxVDRE. The lowest quartile of plasma 25(OH)D compared with the highest, had a multivariate OR of 0.63 (95% CI, 0.48–0.82) for CRC. We did not observe any significant interactions between any GRSs and plasma 25(OH)D. Conclusions: We did not observe evidence for the modification of genetic susceptibility for CRC according to vitamin D status, or evidence that the effect of common CRC risk alleles differed according to their proximity to putative VDR binding sites.
  • Thumbnail Image
    Publication
    Apolipoprotein(a) Size and Lipoprotein(a) Concentration and Future Risk of Angina Pectoris with Evidence of Severe Coronary Atherosclerosis in Men: The Physicians' Health Study
    (American Association for Clinical Chemistry (AACC), 2004) Rifai, Nader; Ma, Jing; Sacks, Frank; Ridker, Paul; Hernandez, W; Stampfer, Meir; Marcovina, S
    The relationship of lipoprotein (a) [Lp(a)] concentrations with risk of coronary heart disease needs clarification, especially for threshold values for increased risk and for possible interactions with LDL-cholesterol concentrations and apolipoprotein (a) [apo(a)] size polymorphism. This study was designed to examine the ability of baseline Lp(a) concentration and apo(a) size to predict future severe angina pectoris in apparently healthy men. METHODS: Baseline Lp(a) concentration and apo(a) size were determined in 195 men who subsequently developed angina and in 195 men who remained free of cardiovascular disease for 5 years. RESULTS: Cases had higher median Lp(a) concentrations than did controls (30.6 vs 22.5 nmol/L; P = 0.02). Lp(a) concentration was predictive of angina [relative risk (RR) from lowest to highest quintiles: 1.0, 1.5, 1.0, 1.8, and 2.6; P for trend = 0.015]. The increased risk was approximately 4-fold (95% confidence interval, 1.4- to 11-fold) among men who had Lp(a) above the 95th percentile (>158 nmol/L). Men with Lp(a) concentrations in the highest quintile and LDL-cholesterol concentrations >1600 mg/L had a 12-fold increased risk (95% confidence interval, 1.5- to 43-fold). Small apo(a) size isoforms also significantly predicted risk of angina (RR for lowest quintile = 4.1; P for trend = 0.004). When the independent effect of Lp(a) concentration and apo(a) size was assessed by including them in the same multivariate model, only the association between apo(a) size and risk remained significant. CONCLUSIONS: High Lp(a) predicts risk of angina, and the risk is substantially increased with high concomitant LDL-cholesterol. Small apo(a) size predicts angina with greater strength and independence than Lp(a) concentration.
  • Thumbnail Image
    Publication
    A meta-analysis of 87,040 individuals identifies 23 new susceptibility loci for prostate cancer
    (2014) Al Olama, Ali Amin; Kote-Jarai, Zsofia; Berndt, Sonja I.; Conti, David V.; Schumacher, Fredrick; Han, Ying; Benlloch, Sara; Hazelett, Dennis J.; Wang, Zhaoming; Saunders, Ed; Leongamornlert, Daniel; Lindstrom, Sara; Jugurnauth-Little, Sara; Dadaev, Tokhir; Tymrakiewicz, Malgorzata; Stram, Daniel O.; Rand, Kristin; Wan, Peggy; Stram, Alex; Sheng, Xin; Pooler, Loreall C.; Park, Karen; Xia, Lucy; Tyrer, Jonathan; Kolonel, Laurence N.; Le Marchand, Loic; Hoover, Robert N.; Machiela, Mitchell J.; Yeager, Merideth; Burdette, Laurie; Chung, Charles C.; Hutchinson, Amy; Yu, Kai; Goh, Chee; Ahmed, Mahbubl; Govindasami, Koveela; Guy, Michelle; Tammela, Teuvo L.J.; Auvinen, Anssi; Wahlfors, Tiina; Schleutker, Johanna; Visakorpi, Tapio; Leinonen, Katri A.; Xu, Jianfeng; Aly, Markus; Donovan, Jenny; Travis, Ruth C.; Key, Tim J.; Siddiq, Afshan; Canzian, Federico; Khaw, Kay-Tee; Takahashi, Atsushi; Kubo, Michiaki; Pharoah, Paul; Pashayan, Nora; Weischer, Maren; Nordestgaard, Borge G.; Nielsen, Sune F.; Klarskov, Peter; Røder, Martin Andreas; Iversen, Peter; Thibodeau, Stephen N.; McDonnell, Shannon K; Schaid, Daniel J; Stanford, Janet L.; Kolb, Suzanne; Holt, Sarah; Knudsen, Beatrice; Coll, Antonio Hurtado; Gapstur, Susan M.; Diver, W. Ryan; Stevens, Victoria L.; Maier, Christiane; Luedeke, Manuel; Herkommer, Kathleen; Rinckleb, Antje E.; Strom, Sara S.; Pettaway, Curtis; Yeboah, Edward D.; Tettey, Yao; Biritwum, Richard B.; Adjei, Andrew A.; Tay, Evelyn; Truelove, Ann; Niwa, Shelley; Chokkalingam, Anand P.; Cannon-Albright, Lisa; Cybulski, Cezary; Wokołorczyk, Dominika; Kluźniak, Wojciech; Park, Jong; Sellers, Thomas; Lin, Hui-Yi; Isaacs, William B.; Partin, Alan W.; Brenner, Hermann; Dieffenbach, Aida Karina; Stegmaier, Christa; Turman, Constance; Giovannucci, Edward; Ma, Jing; Stampfer, Meir; Penney, Kathryn; Mucci, Lorelei; John, Esther M.; Ingles, Sue A.; Kittles, Rick A.; Murphy, Adam B.; Pandha, Hardev; Michael, Agnieszka; Kierzek, Andrzej M.; Blot, William; Signorello, Lisa B; Zheng, Wei; Albanes, Demetrius; Virtamo, Jarmo; Weinstein, Stephanie; Nemesure, Barbara; Carpten, John; Leske, Cristina; Wu, Suh-Yuh; Hennis, Anselm; Kibel, Adam S.; Rybicki, Benjamin A.; Neslund-Dudas, Christine; Hsing, Ann W.; Chu, Lisa; Goodman, Phyllis J.; Klein, Eric A; Zheng, S. Lilly; Batra, Jyotsna; Clements, Judith; Spurdle, Amanda; Teixeira, Manuel R.; Paulo, Paula; Maia, Sofia; Slavov, Chavdar; Kaneva, Radka; Mitev, Vanio; Witte, John S.; Casey, Graham; Gillanders, Elizabeth M.; Seminara, Daniella; Riboli, Elio; Hamdy, Freddie C.; Coetzee, Gerhard A.; Li, Qiyuan; Freedman, Matthew L.; Hunter, David; Muir, Kenneth; Gronberg, Henrik; Neal, David E.; Southey, Melissa; Giles, Graham G.; Severi, Gianluca; Cook, Michael B.; Nakagawa, Hidewaki; Wiklund, Fredrik; Kraft, Phillip; Chanock, Stephen J.; Henderson, Brian E.; Easton, Douglas F.; Eeles, Rosalind A.; Haiman, Christopher A.
    Genome-wide association studies (GWAS) have identified 76 variants associated with prostate cancer risk predominantly in populations of European ancestry. To identify additional susceptibility loci for this common cancer, we conducted a meta-analysis of >10 million SNPs in 43,303prostate cancer cases and 43,737 controls from studies in populations of European, African, Japanese and Latino ancestry. Twenty-three novel susceptibility loci were revealed at P<5×10-8; 15 variants were identified among men of European ancestry, 7 from multiethnic analyses and one was associated with early-onset prostate cancer. These 23 variants, in combination with the known prostate cancer risk variants, explain 33% of the familial risk of the disease in European ancestry populations. These findings provide new regions for investigation into the pathogenesis of prostate cancer and demonstrate the utility of combining ancestrally diverse populations to discover risk loci for disease.
  • Thumbnail Image
    Publication
    Elevated circulating branched chain amino acids are an early event in pancreatic adenocarcinoma development
    (2014) Mayers, Jared R.; Wu, Chen; Clish, Clary B.; Kraft, Phillip; Torrence, Margaret E.; Fiske, Brian P.; Yuan, Chen; Bao, Ying; Townsend, Mary K.; Tworoger, Shelley; Davidson, Shawn M.; Papagiannakopoulos, Thales; Yang, Annan; Dayton, Talya L.; Ogino, Shuji; Stampfer, Meir; Giovannucci, Edward; Qian, Zhi Rong; Rubinson, Douglas; Ma, Jing; Sesso, Howard; Gaziano, John; Cochrane, Barbara B.; Liu, Simin; Wactawski–Wende, Jean; Manson, JoAnn; Pollak, Michael N.; Kimmelman, Alec C.; Souza, Amanda; Pierce, Kerry; Wang, Thomas J.; Gerszten, Robert; Fuchs, Charles; Heiden, Matthew G. Vander; Wolpin, Brian M.
    Most patients with pancreatic ductal adenocarcinoma (PDAC) are diagnosed with advanced disease and survive less than 12 months1. PDAC has been linked with obesity and glucose intolerance2-4, but whether changes in circulating metabolites are associated with early cancer progression is unknown. To better understand metabolic derangements associated with early disease, we profiled metabolites in prediagnostic plasma from pancreatic cancer cases and matched controls from four prospective cohort studies. We find that elevated plasma levels of branched chain amino acids (BCAAs) are associated with a greater than 2–fold increased risk of future pancreatic cancer diagnosis. This elevated risk was independent of known predisposing factors, with the strongest association observed among subjects with samples collected 2 to 5 years prior to diagnosis when occult disease is likely present. We show that plasma BCAAs are also elevated in mice with early stage pancreatic cancers driven by mutant Kras expression, and that breakdown of tissue protein accounts for the increase in plasma BCAAs that accompanies early stage disease. Together, these findings suggest that increased whole–body protein breakdown is an early event in development of PDAC.
  • Thumbnail Image
    Publication
    Mannose-Binding Lectin 2 Gene and Risk of Adult Glioma
    (Public Library of Science, 2013) Michaud, Dominique S.; Siddiq, Afshan; Cox, David G.; Backes, Danielle M.; Calboli, Federico C. F.; Sughrue, Michael E.; Gaziano, John; Ma, Jing; Stampfer, Meir; Tworoger, Shelley; Hunter, David; Camargo, Carlos; Parsa, Andrew T.
    Background and Aims The immune system is likely to play a key role in the etiology of gliomas. Genetic polymorphisms in the mannose-binding lectin gene, a key activator in the lectin complement pathway, have been associated with risk of several cancers. Methods: To examine the role of the lectin complement pathway, we combined data from prospectively collected cohorts with available DNA specimens. Using a nested case-control design, we genotyped 85 single nucleotide polymorphisms (SNPs) in 9 genes in the lectin complement pathway and 3 additional SNPs in MBL2 were tested post hoc). Initial SNPs were selected using tagging SNPs for haplotypes; the second group of SNPs for MBL2 was selected based on functional SNPs related to phenotype. Associations were examined using logistic regression analysis. All statistical tests were two-sided. Nominal p-values are presented and are not corrected for multiple comparisons. Results: A total of 143 glioma cases and 419 controls were available for this analysis. Statistically significant associations were observed for two SNPs in the mannose-binding lectin 2 (ML2) gene and risk of glioma (rs1982266 and rs1800450, test for trend p = 0.003 and p = 0.04, respectively, using the additive model). One of these SNPs, rs1800450, was associated with a 58% increase in glioma risk among those carrying one or two mutated alleles (odds ratio = 1.58, 95% confidence interval = 0.99–2.54), compared to those homozygous for the wild type allele. Conclusions: Overall, our findings suggest that MBL may play a role in the etiology of glioma. Future studies are needed to confirm these findings which may be due to chance, and if reproduced, to determine mechanisms that link glioma pathogenesis with the MBL complement pathway.
  • Thumbnail Image
    Publication
    Y Chromosome Haplogroups and Prostate Cancer in Populations of European and Ashkenazi Jewish Ancestry
    (Springer-Verlag, 2012) Wang, Zhaoming; Parikh, Hemang; Jia, Jinping; Yeager, Meredith; Jacobs, Kevin B.; Hutchinson, Amy; Burdett, Laurie; Ghosh, Arpita; Thun, Michael J.; Gapstur, Susan M.; Virtamo, Jarmo; Albanes, Demetrius; Cancel-Tassin, Geraldine; Valeri, Antoine; Cussenot, Olivier; Offit, Kenneth; Dutra-Clarke, Ana; Kirchhoff, Tomas; Alavanja, Michael; Freeman, Laura B.; Koutros, Stella; Hoover, Robert; Berndt, Sonja I.; Hayes, Richard B.; Agalliu, Ilir; Burk, Robert D.; Wacholder, Sholom; Thomas, Gilles; Amundadottir, Laufey; Myers, Timothy; Giovannucci, Edward; Ma, Jing; Stampfer, Meir; Gaziano, John; Hunter, David; Diver, W. Ryan
    Genetic variation on the Y chromosome has not been convincingly implicated in prostate cancer risk. To comprehensively analyze the role of inherited Y chromosome variation in prostate cancer risk in individuals of European ancestry, we genotyped 34 binary Y chromosome markers in 3,995 prostate cancer cases and 3,815 control subjects drawn from four studies. In this set, we identified nominally significant association between a rare haplogroup, E1b1b1c, and prostate cancer in stage I (P = 0.012, OR = 0.51; 95% confidence interval 0.30–0.87). Population substructure of E1b1b1c carriers suggested Ashkenazi Jewish ancestry, prompting a replication phase in individuals of both European and Ashkenazi Jewish ancestry. The association was not significant for prostate cancer overall in studies of either Ashkenazi Jewish (1,686 cases and 1,597 control subjects) or European (686 cases and 734 control subjects) ancestry (\(P_{meta}\) = 0.078), but a meta-analysis of stage I and II studies revealed a nominally significant association with prostate cancer risk (\(P_{meta}\) = 0.010, OR = 0.77; 95% confidence interval 0.62–0.94). Comparing haplogroup frequencies between studies, we noted strong similarities between those conducted in the US and France, in which the majority of men carried R1 haplogroups, resembling Northwestern European populations. On the other hand, Finns had a remarkably different haplogroup distribution with a preponderance of N1c and I1 haplogroups. In summary, our results suggest that inherited Y chromosome variation plays a limited role in prostate cancer etiology in European populations but warrant follow-up in additional large and well characterized studies of multiple ethnic backgrounds.
  • Thumbnail Image
    Publication
    Blood Donation and Colorectal Cancer Incidence and Mortality in Men
    (Public Library of Science, 2012) Zhang, Xuehong; Ma, Jing; Wu, Kana; Chan, Andrew; Fuchs, Charles; Giovannucci, Edward
    Background: Although blood donations may reduce body iron stores, to date, prospective data on frequent blood donation and colorectal cancer risk are limited. Methodology/Principal Findings: We tested whether frequent blood donation is associated with a lower risk of colorectal cancer in the Health Professionals Follow-up Study. We prospectively followed 35,121men who provide the information on lifetime number of blood donations in 1992 through 2008. Serum ferritin levels were measured in a random sample of 305 men. Cox proportional hazard regression models were used to calculate the multivariable relative risks (RRs, 95%CIs) after adjusting for age and other established colorectal cancer risk factors. We documented 684 incident colorectal cancer cases and 224 deaths from colorectal cancer. The mean serum ferritin levels varied from 178 µg/L for men who did not donate blood to 98 µg/L for men who had at least 30 donations. Age-adjusted results for both incidence and mortality were essentially the same as the multivariable-adjusted results. Comparing with non-donors, the multivariable RRs (95%CIs) for colorectal cancer incidence were 0.92 (0.77, 1.11) for 1–5 donation, 0.85 (0.64, 1.11) for 6–9 donations, 0.96 (0.73, 1.26) for 10–19 donations, 0.91 (0.63, 1.32) for 20–29 donations, and 0.97 (0.68, 1.38) for at least 30 donations (Ptrend = 0.92). The multivariable RRs for colorectal cancer mortality were 0.99 (0.72, 1.36) for 1–5 donation, 0.93 (0.57, 1.51) for 6–9 donations, 0.85 (0.50, 1.42) for 10–19 donations, and 1.14 (0.72, 1.83) for at least 20 donations (Ptrend = 0.82). The results did not vary by cancer sub-sites, intake levels of total iron, heme iron, or family history of colorectal cancer. Conclusions/Significance: Frequent blood donations were not associated with colorectal cancer incidence and mortality in men. Our results do not support an important role of body iron stores in colorectal carcinogenesis.
  • Thumbnail Image
    Publication
    Magnesium intake, plasma C-peptide, and colorectal cancer incidence in US women: a 28-year follow-up study
    (Nature Publishing Group, 2012) Zhang, Xiaoxiao; Giovannucci, Edward; Wu, Kunling; Smith-Warner, Stephanie; Fuchs, Charles; Pollak, Martin; Willett, Walter; Ma, Jing
    Background: Laboratory studies suggest a possible role of magnesium intake in colorectal carcinogenesis but epidemiological evidence is inconclusive. Method: We tested magnesium–colorectal cancer hypothesis in the Nurses' Health Study, in which 85 924 women free of cancer in 1980 were followed until June 2008. Cox proportional hazards regression models were used to estimate multivariable relative risks (MV RRs, 95% confidence intervals). Results: In the age-adjusted model, magnesium intake was significantly inversely associated with colorectal cancer risk; the RRs from lowest to highest decile of total magnesium intake were 1.0 (ref), 0.93, 0.81, 0.72, 0.74, 0.77, 0.72, 0.75, 0.80, and 0.67 (Ptrend<0.001). However, in the MV model adjusted for known dietary and non-dietary risk factors for colorectal cancer, the association was significantly attenuated; the MV RRs were 1.0 (ref), 0.96, 0.85, 0.78, 0.82, 0.86, 0.84, 0.91, 1.02, and 0.93 (Ptrend=0.77). Similarly, magnesium intakes were significantly inversely associated with concentrations of plasma C-peptide in age-adjusted model (Ptrend=0.002) but not in multivariate-adjusted model (Ptrend=0.61). Results did not differ by subsite or modified by calcium intakes or body mass index. Conclusion: These prospective results do not support an independent association of magnesium intake with either colorectal cancer risk or plasma C-peptide levels in women.
  • Thumbnail Image
    Publication
    Genetic Variation in the HSD17B1 Gene and Risk of Prostate Cancer
    (Public Library of Science, 2005) Kraft, Peter; Pharoah, Paul; Chanock, Stephen J; Albanes, Demetrius; Kolonel, Laurence N; Hayes, Richard B; Andriole, Gerald; Berg, Christine; Boeing, Heiner; Burtt, Noel P; Bueno-de-Mesquita, Bas; Calle, Eugenia E; Cann, Howard; Canzian, Federico; Crawford, David E; Dunning, Alison M; Feigelson, Heather S; Gonzalez, Carlos Alberto; Haiman, Christopher A; Hallmans, Goran; Henderson, Brian E; Kaaks, Rudolf; Key, Timothy; Marchand, Loic Le; Overvad, Kim; Palli, Domenico; Pike, Malcolm C; Riboli, Elio; Rodriguez, Carmen; Setiawan, Wendy V; Stram, Daniel O; Thomas, Gilles; Thun, Michael J; Travis, Ruth; Trichopoulou, Antonia; Virtamo, Jarmo; Wacholder, Sholom; Altshuler, David; Chen, Yin-Ching; Freedman, Matthew; Gaziano, John; Giovannucci, Edward; Hirschhorn, Joel; Hunter, David; Ma, Jing; Stampfer, Meir
    Steroid hormones are believed to play an important role in prostate carcinogenesis, but epidemiological evidence linking prostate cancer and steroid hormone genes has been inconclusive, in part due to small sample sizes or incomplete characterization of genetic variation at the locus of interest. Here we report on the results of a comprehensive study of the association between HSD17B1 and prostate cancer by the Breast and Prostate Cancer Cohort Consortium, a large collaborative study. HSD17B1 encodes 17β-hydroxysteroid dehydrogenase 1, an enzyme that converts dihydroepiandrosterone to the testosterone precursor Δ5-androsterone-3β,17β-diol and converts estrone to estradiol. The Breast and Prostate Cancer Cohort Consortium researchers systematically characterized variation in HSD17B1 by targeted resequencing and dense genotyping; selected haplotype-tagging single nucleotide polymorphisms (htSNPs) that efficiently predict common variants in U.S. and European whites, Latinos, Japanese Americans, and Native Hawaiians; and genotyped these htSNPs in 8,290 prostate cancer cases and 9,367 study-, age-, and ethnicity-matched controls. We found no evidence that HSD17B1 htSNPs (including the nonsynonymous coding SNP S312G) or htSNP haplotypes were associated with risk of prostate cancer or tumor stage in the pooled multiethnic sample or in U.S. and European whites. Analyses stratified by age, body mass index, and family history of disease found no subgroup-specific associations between these HSD17B1 htSNPs and prostate cancer. We found significant evidence of heterogeneity in associations between HSD17B1 haplotypes and prostate cancer across ethnicity: one haplotype had a significant (p < 0.002) inverse association with risk of prostate cancer in Latinos and Japanese Americans but showed no evidence of association in African Americans, Native Hawaiians, or whites. However, the smaller numbers of Latinos and Japanese Americans in this study makes these subgroup analyses less reliable. These results suggest that the germline variants in HSD17B1 characterized by these htSNPs do not substantially influence the risk of prostate cancer in U.S. and European whites.