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1. Do GWAS-Identified Risk Variants for Chronic Lymphocytic Leukemia Influence Overall Patient Survival and Disease Progression?

Author: Cabrera-Serrano, A.J., Sánchez-Maldonado, J.M., Horst, R, Macauda, A., García-Martín, P., Benavente, Y., Landi, S., Clay-Gilmour, A., Niazi, Y., Espinet, B., Rodríguez-Sevilla, J.J., Pérez, E.M., Maffei, R., Blanco, G., Giaccherini, M., Cerhan, J.R., Marasca, R., López-Nevot, M.Á., Chen-Liang, T., Thomsen, H., Gámez, I., Campa, D., Moreno, V., Sanjosé, S. de, Marcos-Gragera, R., García-Álvarez, M., Dierssen-Sotos, T., Jerez, A., Butrym, A., Norman, A.D., Luppi, M., Slager, S.L., Hemminki, K., Li, Y., Berndt, S.I., Casabonne, D., Alcoceba, M., Puiggros, A., Netea, M.G., Försti, A., Canzian, F., Sainz, J., Cabrera-Serrano, A.J., Sánchez-Maldonado, J.M., Horst, R, Macauda, A., García-Martín, P., Benavente, Y., Landi, S., Clay-Gilmour, A., Niazi, Y., Espinet, B., Rodríguez-Sevilla, J.J., Pérez, E.M., Maffei, R., Blanco, G., Giaccherini, M., Cerhan, J.R., Marasca, R., López-Nevot, M.Á., Chen-Liang, T., Thomsen, H., Gámez, I., Campa, D., Moreno, V., Sanjosé, S. de, Marcos-Gragera, R., García-Álvarez, M., Dierssen-Sotos, T., Jerez, A., Butrym, A., Norman, A.D., Luppi, M., Slager, S.L., Hemminki, K., Li, Y., Berndt, S.I., Casabonne, D., Alcoceba, M., Puiggros, A., Netea, M.G., Försti, A., Canzian, F., and Sainz, J.
Abstract: Contains fulltext : 292738.pdf (Publisher’s version ) (Open Access), Chronic lymphocytic leukemia (CLL) is the most common leukemia among adults worldwide. Although genome-wide association studies (GWAS) have uncovered the germline genetic component underlying CLL susceptibility, the potential use of GWAS-identified risk variants to predict disease progression and patient survival remains unexplored. Here, we evaluated whether 41 GWAS-identified risk variants for CLL could influence overall survival (OS) and disease progression, defined as time to first treatment (TTFT) in a cohort of 1039 CLL cases ascertained through the CRuCIAL consortium. Although this is the largest study assessing the effect of GWAS-identified susceptibility variants for CLL on OS, we only found a weak association of ten single nucleotide polymorphisms (SNPs) with OS (p < 0.05) that did not remain significant after correction for multiple testing. In line with these results, polygenic risk scores (PRSs) built with these SNPs in the CRuCIAL cohort showed a modest association with OS and a low capacity to predict patient survival, with an area under the receiver operating characteristic curve (AUROC) of 0.57. Similarly, seven SNPs were associated with TTFT (p < 0.05); however, these did not reach the multiple testing significance threshold, and the meta-analysis with previous published data did not confirm any of the associations. As expected, PRSs built with these SNPs showed reduced accuracy in prediction of disease progression (AUROC = 0.62). These results suggest that susceptibility variants for CLL do not impact overall survival and disease progression in CLL patients.
Published: 2023

2. Acortamiento cubital. Contribución del sistema guiado para osteotomía y síntesis

Author: Oteo, J.A. and Merino, P. Benavente y P.
Published: 2015
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3. Common genetic polymorphisms contribute to the association between chronic lymphocytic leukaemia and non-melanoma skin cancer

Author: Besson, C., Moore, A., Vajdic, C.M., de Sanjose, S., Camp, N.J., Smedby, K.E., Shanafelt, T.D., Morton, L.M., Brewer, J.D., Zablotska, L., Chung, C.C., Teras, L.R., Kleinstern, G., Monnereau, A., Kane, E., Benavente, Y., Purdue, M.P., Birmann, B.M., Link, B.K., Vermeulen, R.C.H., Spinelli, J.J., Albanes, D., Arslan, A.A., Miligi, L., Molina, T.J., Skibola, C.F., Cozen, W., Staines, A., Caporaso, N.E., Giles, G.G., Southey, M.C., Milne, R.L., Tinker, L.F., Severson, R.K., Melbye, M., Adami, H.-O., Glimelius, B., Bracci, P.M., Conde, L., Glenn, M., Curtin, K., Lan, Q., Zheng, T., Weinstein, S., Brooks-Wilson, A.R., Diver, W.R., Clavel, J., Vineis, P., Weiderpass, E., Becker, N., Boffetta, P., Brennan, P., Foretova, L., Maynadie, M., Weinberg, J.B., Sanna, S., Gambelunghe, A., Jackson, R.D., Hjalgrim, H., North, K.E., McKay, J., Offit, K., Vijai, J., Nieters, A., Engels, E.A., Chanock, S.J., Rothman, N., Cerhan, J.R., Slager, S.L., Han, J., Berndt, S.I., IRAS OH Epidemiology Chemical Agents, and dIRAS RA-2
Subjects: 0301 basic medicine, Oncology, medicine.medical_specialty, Skin Neoplasms, Epidemiology, Chronic lymphocytic leukemia, Single-nucleotide polymorphism, Polymorphism, Single Nucleotide, 03 medical and health sciences, 0302 clinical medicine, Polygenic risk score, immune system diseases, Risk Factors, Polymorphism (computer science), hemic and lymphatic diseases, Internal medicine, Pleiotropism, Genetics, medicine, Genetic predisposition, Humans, Basal cell carcinoma, neoplasms, Pleiotropy, business.industry, General Medicine, Odds ratio, medicine.disease, Leukemia, Lymphocytic, Chronic, B-Cell, NMSC, 030104 developmental biology, Carcinoma, Basal Cell, 030220 oncology & carcinogenesis, Carcinoma, Squamous Cell, Skin cancer, business, CLL
Abstract: Background Epidemiological studies have demonstrated a positive association between chronic lymphocytic leukaemia (CLL) and non-melanoma skin cancer (NMSC). We hypothesized that shared genetic risk factors between CLL and NMSC could contribute to the association observed between these diseases. Methods We examined the association between (i) established NMSC susceptibility loci and CLL risk in a meta-analysis including 3100 CLL cases and 7667 controls and (ii) established CLL loci and NMSC risk in a study of 4242 basal cell carcinoma (BCC) cases, 825 squamous cell carcinoma (SCC) cases and 12802 controls. Polygenic risk scores (PRS) for CLL, BCC and SCC were constructed using established loci. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs). Results Higher CLL-PRS was associated with increased BCC risk (OR4th-quartile-vs-1st-quartile = 1.13, 95% CI: 1.02–1.24, Ptrend = 0.009), even after removing the shared 6p25.3 locus. No association was observed with BCC-PRS and CLL risk (Ptrend = 0.68). These findings support a contributory role for CLL in BCC risk, but not for BCC in CLL risk. Increased CLL risk was observed with higher SCC-PRS (OR4th-quartile-vs-1st-quartile = 1.22, 95% CI: 1.08–1.38, Ptrend = 1.36 × 10–5), which was driven by shared genetic susceptibility at the 6p25.3 locus. Conclusion These findings highlight the role of pleiotropy regarding the pathogenesis of CLL and NMSC and shows that a single pleiotropic locus, 6p25.3, drives the observed association between genetic susceptibility to SCC and increased CLL risk. The study also provides evidence that genetic susceptibility for CLL increases BCC risk.
Published: 2021

4. Validation and functional characterization of GWAS-identified variants for chronic lymphocytic leukemia: a CRuCIAL study

Author: García-Martín, P., Díez, A.M., Maldonado, J.M.S., Serrano, A.J.C., Horst, R. ter, Benavente, Y., Landi, S., Macauda, A., Clay-Gilmour, A., Hernández-Mohedo, F., Niazi, Y., González-Sierra, P., Espinet, B., Rodríguez-Sevilla, J.J., Maffei, R., Blanco, G., Giaccherini, M., Puiggros, A., Cerhan, J., Marasca, R., Cañadas-Garre, M., López-Nevot, M., Chen-Liang, T., Thomsen, H., Gámez, I., Moreno, V., Marcos-Gragera, R., García-Álvarez, M., Llorca, J., Jerez, A., Berndt, S., Butrym, A., Norman, A.D., Casabonne, D., Luppi, M., Slager, S.L., Hemminki, K., Li, Y., Alcoceba, M., Campa, D., Canzian, F., Sanjosé, S. de, Försti, A., Netea, M.G., Jurado, M., Sainz, J., García-Martín, P., Díez, A.M., Maldonado, J.M.S., Serrano, A.J.C., Horst, R. ter, Benavente, Y., Landi, S., Macauda, A., Clay-Gilmour, A., Hernández-Mohedo, F., Niazi, Y., González-Sierra, P., Espinet, B., Rodríguez-Sevilla, J.J., Maffei, R., Blanco, G., Giaccherini, M., Puiggros, A., Cerhan, J., Marasca, R., Cañadas-Garre, M., López-Nevot, M., Chen-Liang, T., Thomsen, H., Gámez, I., Moreno, V., Marcos-Gragera, R., García-Álvarez, M., Llorca, J., Jerez, A., Berndt, S., Butrym, A., Norman, A.D., Casabonne, D., Luppi, M., Slager, S.L., Hemminki, K., Li, Y., Alcoceba, M., Campa, D., Canzian, F., Sanjosé, S. de, Försti, A., Netea, M.G., Jurado, M., and Sainz, J.
Abstract: Contains fulltext : 251927.pdf (Publisher’s version ) (Open Access)
Published: 2022

5. High-risk subtypes of chronic lymphocytic leukemia are detectable as early as 16 years prior to diagnosis

Author: Kolijn, P.M. Hosnijeh, F.S. Späth, F. Hengeveld, P.J. Agathangelidis, A. Saleh, M. Casabonne, D. Benavente, Y. Jerkeman, M. Agudo, A. Barricarte, A. Besson, C. Sánchez, M.-J. Chirlaque, M.-D. Masala, G. Sacerdote, C. Grioni, S. Schulze, M.B. Nieters, A. Engelfriet, P. Hultdin, M. McKay, J.D. Vermeulen, R.C.H. Langerak, A.W.
Subjects: immune system diseases, hemic and lymphatic diseases
Abstract: Chronic lymphocytic leukemia (CLL) is preceded by monoclonal B-cell lymphocytosis (MBL), a CLL precursor state with a prevalence of up to 12% in aged individuals; however, the duration of MBL and the mechanisms of its evolution to CLL remain largely unknown. In this study, we sequenced the B-cell receptor (BcR) immunoglobulin heavy chain (IGH) gene repertoire of 124 patients with CLL and 118 matched controls in blood samples taken up to 22 years prior to diagnosis. Significant skewing in the BcR IGH gene repertoire was detected in the majority of patients, even before the occurrence of lymphocytosis and irrespective of the clonotypic IGH variable gene somatic hypermutation status. Furthermore, we identified dominant clonotypes belonging to major stereotyped subsets associated with poor prognosis up to 16 years before diagnosis in 14 patients with CLL. In 22 patients with longitudinal samples, the skewing of the BcR IGH gene repertoire increased significantly over time to diagnosis or remained stable at high levels. For 14 of 16 patients with available samples at diagnosis, the CLL clonotype was already present in the prediagnostic samples. Overall, our data indicate that the preclinical phase of CLL could be longer than previously thought, even in adverse-prognostic cases. © 2022 American Society of Hematology
Published: 2022

6. Exposure to Non-Arsenic Pesticides is Associated with Lymphoma among Farmers in Spain

Author: van Balen, E., Font, R., Cavallé, N., Font, L., Garcia-Villanueva, M., Benavente, Y., Brennan, P., and de Sanjose, S.
Published: 2006
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7. [Family history of first degree as a risk factor for colorectal cancer]

Author: Rubín-García M, Martín V, Vitelli-Storelli F, Moreno V, Aragonés N, Ardanaz E, Alonso-Molero J, Jiménez-Moleón JJ, Amiano P, Fernández-Tardón G, Molina-Barceló A, Alguacil J, Dolores-Chirlaque M, Álvarez-Álvarez L, Pérez-Gómez B, Dierssen-Sotos T, Olmedo-Requena R, Guevara M, Fernández-Villa T, Pollán M, and Benavente Y
Subjects: Factor de riesgo, MCCSpain, Family history, Antecedentes familiares, MCC-Spain, Middle Aged, Colorectal cancer, Case and control, Risk Factors, Spain, Odds Ratio, Humans, Cáncer colorrectal, Family, Risk factor, Casos y controles, Colorectal Neoplasms
Abstract: Objective: To evaluate the association between first-degree family history and colorectal cancer (CRC). Method: We analyzed data from 2857 controls and 1360 CRC cases, collected in the MCC-Spain project. The adjusted odds ratio (OR) and 95% confidence interval (95% CI) of association with the family history of CRC was estimated by non-conditional logistic regression. Result: First-degree relatives doubled the risk of CRC (OR: 2.19; 95% CI: 1.80-2.66), increasing in those with two or more (OR: 4.22; 95% CI: 2.29-7.78) and in those whose relatives were diagnosed before 50 years (OR: 3.24; 95% CI: 1.52-6.91). Regarding the association of the family history with the location, no significant differences were observed between colon and rectum, but there were in the relation of these with the age of diagnosis, having more relatives those diagnosed before 50 years (OR: 4.79; 95% CI: 2.65-8.65). Conclusions: First-degree relatives of CRC increase the chances of developing this tumor, they also increase when the relative is diagnosed at an early age. Therefore, it must be a target population on which to carry out prevention measures. (C) 2021 SESPAS. Published by Elsevier Espana, S.L.U.
Published: 2021

8. 245 The significance of surgical assessment in oncological outcomes after radical hysterectomy for early-stage cervical cancer. A multicenter study

Author: Fernandez-Gonzalez, S, primary, Barahona, M, additional, Gil-Moreno, A, additional, Gómez-Hidalgo, NR, additional, Diaz-Feijoo, B, additional, Coronado, P, additional, González, V, additional, Casajuana, A, additional, Silvan, JM, additional, Melero, L, additional, Martinez, MA, additional, Hilario de la Rosa, J, additional, Lobo, I, additional, Beiro, E, additional, Frias-Gomez, J, additional, Benavente, Y, additional, Ortega, C, additional, Martinez, E, additional, Marti, L, additional, and Ponce, J, additional
Published: 2021
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9. Common genetic polymorphisms contribute to the association between chronic lymphocytic leukaemia and non-melanoma skin cancer

Author: IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Besson, C., Moore, A., Vajdic, C.M., de Sanjose, S., Camp, N.J., Smedby, K.E., Shanafelt, T.D., Morton, L.M., Brewer, J.D., Zablotska, L., Chung, C.C., Teras, L.R., Kleinstern, G., Monnereau, A., Kane, E., Benavente, Y., Purdue, M.P., Birmann, B.M., Link, B.K., Vermeulen, R.C.H., Spinelli, J.J., Albanes, D., Arslan, A.A., Miligi, L., Molina, T.J., Skibola, C.F., Cozen, W., Staines, A., Caporaso, N.E., Giles, G.G., Southey, M.C., Milne, R.L., Tinker, L.F., Severson, R.K., Melbye, M., Adami, H.-O., Glimelius, B., Bracci, P.M., Conde, L., Glenn, M., Curtin, K., Lan, Q., Zheng, T., Weinstein, S., Brooks-Wilson, A.R., Diver, W.R., Clavel, J., Vineis, P., Weiderpass, E., Becker, N., Boffetta, P., Brennan, P., Foretova, L., Maynadie, M., Weinberg, J.B., Sanna, S., Gambelunghe, A., Jackson, R.D., Hjalgrim, H., North, K.E., McKay, J., Offit, K., Vijai, J., Nieters, A., Engels, E.A., Chanock, S.J., Rothman, N., Cerhan, J.R., Slager, S.L., Han, J., Berndt, S.I., IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Besson, C., Moore, A., Vajdic, C.M., de Sanjose, S., Camp, N.J., Smedby, K.E., Shanafelt, T.D., Morton, L.M., Brewer, J.D., Zablotska, L., Chung, C.C., Teras, L.R., Kleinstern, G., Monnereau, A., Kane, E., Benavente, Y., Purdue, M.P., Birmann, B.M., Link, B.K., Vermeulen, R.C.H., Spinelli, J.J., Albanes, D., Arslan, A.A., Miligi, L., Molina, T.J., Skibola, C.F., Cozen, W., Staines, A., Caporaso, N.E., Giles, G.G., Southey, M.C., Milne, R.L., Tinker, L.F., Severson, R.K., Melbye, M., Adami, H.-O., Glimelius, B., Bracci, P.M., Conde, L., Glenn, M., Curtin, K., Lan, Q., Zheng, T., Weinstein, S., Brooks-Wilson, A.R., Diver, W.R., Clavel, J., Vineis, P., Weiderpass, E., Becker, N., Boffetta, P., Brennan, P., Foretova, L., Maynadie, M., Weinberg, J.B., Sanna, S., Gambelunghe, A., Jackson, R.D., Hjalgrim, H., North, K.E., McKay, J., Offit, K., Vijai, J., Nieters, A., Engels, E.A., Chanock, S.J., Rothman, N., Cerhan, J.R., Slager, S.L., Han, J., and Berndt, S.I.
Published: 2021

10. Association between anthropometry and lifestyle factors and risk of B-cell lymphoma: An exposome-wide analysis

Author: Saberi Hosnijeh, F, Casabonne, D, Nieters, A, Solans, M, Naudin, S, Ferrari, P, Mckay, JD, Benavente, Y, Weiderpass, E, Freisling, H, Severi, G, Boutron Ruault, M-C, Besson, C, Agnoli, C, Masala, G, Sacerdote, C, Tumino, R, Huerta, JM, Amiano, P, Rodriguez-Barranco, M, Bonet, C, Barricarte, A, Christakoudi, S, Knuppel, A, Bueno-de-Mesquita, B, Schulze, MB, Kaaks, R, Canzian, F, Spath, F, Jerkeman, M, Rylander, C, Tjonneland, A, Olsen, A, Borch, KB, Vermeulen, R, Saberi Hosnijeh, F, Casabonne, D, Nieters, A, Solans, M, Naudin, S, Ferrari, P, Mckay, JD, Benavente, Y, Weiderpass, E, Freisling, H, Severi, G, Boutron Ruault, M-C, Besson, C, Agnoli, C, Masala, G, Sacerdote, C, Tumino, R, Huerta, JM, Amiano, P, Rodriguez-Barranco, M, Bonet, C, Barricarte, A, Christakoudi, S, Knuppel, A, Bueno-de-Mesquita, B, Schulze, MB, Kaaks, R, Canzian, F, Spath, F, Jerkeman, M, Rylander, C, Tjonneland, A, Olsen, A, Borch, KB, and Vermeulen, R
Abstract: To better understand the role of individual and lifestyle factors in human disease, an exposome-wide association study was performed to investigate within a single-study anthropometry measures and lifestyle factors previously associated with B-cell lymphoma (BCL). Within the European Prospective Investigation into Cancer and nutrition study, 2402 incident BCL cases were diagnosed from 475 426 participants that were followed-up on average 14 years. Standard and penalized Cox regression models as well as principal component analysis (PCA) were used to evaluate 84 exposures in relation to BCL risk. Standard and penalized Cox regression models showed a positive association between anthropometric measures and BCL and multiple myeloma/plasma cell neoplasm (MM). The penalized Cox models additionally showed the association between several exposures from categories of physical activity, smoking status, medical history, socioeconomic position, diet and BCL and/or the subtypes. PCAs confirmed the individual associations but also showed additional observations. The PC5 including anthropometry, was positively associated with BCL, diffuse large B-cell lymphoma (DLBCL) and MM. There was a significant positive association between consumption of sugar and confectionary (PC11) and follicular lymphoma risk, and an inverse association between fish and shellfish and Vitamin D (PC15) and DLBCL risk. The PC1 including features of the Mediterranean diet and diet with lower inflammatory score showed an inverse association with BCL risk, while the PC7, including dairy, was positively associated with BCL and DLBCL risk. Physical activity (PC10) was positively associated with DLBCL risk among women. This study provided informative insights on the etiology of BCL.
Published: 2021

11. Family history and gastric cancer risk: A pooled investigation in the stomach cancer pooling (STOP) project consortium

Author: Vitelli-Storelli, F., Rubin-Garcia, M., Pelucchi, C., Benavente, Y., Bonzi, R., Rota, M., Palli, D., Ferraroni, M., Lunet, Nuno Miguel De Sousa, Morais, S., Ye, W., Plymoth, A., Malekzadeh, R., Tsugane, S., Hidaka, A., Aragones, N., Castano-Vinyals, G., Zaridze, D. G., Maximovich, D., Vioque, J., Garcia-de-la-Hera, M., Zhang, Z. -F., Hamada, G. S., Pakseresht, M., Pourfarzi, F., Mu, L., Boccia, Stefania, Pastorino, Roberta, Yu, G. -P., Lagiou, A., Lagiou, P., Negri, E., Vecchia, C. L., Martin, V., Lunet N., Boccia S. (ORCID:0000-0002-1864-749X), Pastorino R. (ORCID:0000-0001-5013-0733), Vitelli-Storelli, F., Rubin-Garcia, M., Pelucchi, C., Benavente, Y., Bonzi, R., Rota, M., Palli, D., Ferraroni, M., Lunet, Nuno Miguel De Sousa, Morais, S., Ye, W., Plymoth, A., Malekzadeh, R., Tsugane, S., Hidaka, A., Aragones, N., Castano-Vinyals, G., Zaridze, D. G., Maximovich, D., Vioque, J., Garcia-de-la-Hera, M., Zhang, Z. -F., Hamada, G. S., Pakseresht, M., Pourfarzi, F., Mu, L., Boccia, Stefania, Pastorino, Roberta, Yu, G. -P., Lagiou, A., Lagiou, P., Negri, E., Vecchia, C. L., Martin, V., Lunet N., Boccia S. (ORCID:0000-0002-1864-749X), and Pastorino R. (ORCID:0000-0001-5013-0733)
Abstract: Research is still required to establish the relationship between family history (FH) and gastric cancer (GC) in relation to different histological types and anatomical sites. The present work aimed to examine the influence of first-degree FH on the risk of GC, also according to the GC location and histological type, including 5946 cases and 12,776 controls from 17 studies of 11 countries in three continents participating in the Stomach Cancer Pooling (StoP) Project consortium. This analysis confirms the effect of FH on the risk of GC, reporting an approximately doubled risk, and provides further quantification of the risk of GC according to the subsite and histotype. Although there is a clear relationship between family history (FH) and the risk of gastric cancer (GC), quantification is still needed in relation to different histological types and anatomical sites, and in strata of covariates. The objective was to analyze the risk of GC according to first-degree FH in a uniquely large epidemiological consortium of GC. This investigation includes 5946 cases and 12,776 controls from 17 studies of the Stomach Cancer Pooling (StoP) Project consortium. Summary odds ratios (OR) and the corresponding 95% confidence intervals (CIs) were calculated by pooling study-specific ORs using fixed-effect model meta-analysis techniques. Stratified analyses were carried out by sex, age, tumor location and histological type, smoking habit, socioeconomic status, alcohol intake and fruit consumption. The pooled OR for GC was 1.84 (95% CI: 1.64-2.04; I2 = 6.1%, P heterogeneity = 0.383) in subjects with vs. those without first-degree relatives with GC. No significant differences were observed among subgroups of sex, age, geographic area or study period. Associations tended to be stronger for non-cardia (OR = 1.82; 95% CI: 1.59-2.05 for subjects with FH) than for cardia GC (OR = 1.38; 95% CI: 0.98-1.77), and for the intestinal (OR = 1.92; 95% CI: 1.62-2.23) than for the diffuse histotype (OR
Published: 2021

12. Lipid trait variants and the risk of non-hodgkin lymphoma subtypes: a mendelian randomization study

Author: Kleinstern, G., Camp, N.J., Berndt, S.I., Birmann, B.M., Nieters, A., Bracci, P.M., McKay, J.D., Ghesquieres, H., Lan, Q., Hjalgrim, H., Benavente, Y., Monnereau, A., Purdue, M.P., Zeleniuch-Jacquotte, A., Giles, G.G., Vermeulen, R., Cocco, P., Albanes, D., Teras, L.R., Brooks-Wilson, A.R., Vajdic, C.M., Kane, E., Caporaso, N.E., Smedby, K.E., Salles, G., Vijai, J., Chanock, S.J., Skibola, C.F., Rothman, N., Slager, S.L., Cerhan, J.R., IRAS OH Epidemiology Chemical Agents, and dIRAS RA-2
Abstract: Background: Lipid traits have been inconsistently linked to risk of non-Hodgkin lymphoma (NHL). We examined the association of genetically predicted lipid traits with risk of diffuse large B-cell lymphoma (DLBCL), chronic lymphocytic leukemia (CLL), follicular lymphoma (FL), and marginal zone lymphoma (MZL) using Mendelian randomization (MR) analysis. Methods: Genome-wide association study data from the InterLymph Consortium were available for 2,661 DLBCLs, 2,179 CLLs, 2,142 FLs, 824 MZLs, and 6,221 controls. SNPs associated (P < 5 × 10−8) with high-density lipoprotein (HDL, n = 164), low-density lipoprotein (LDL, n = 137), total cholesterol (TC, n = 161), and triglycerides (TG, n = 123) were used as instrumental variables (IV), explaining 14.6%, 27.7%, 16.8%, and 12.8% of phenotypic variation, respectively. Associations between each lipid trait and NHL subtype were calculated using the MR inverse variance–weighted method, estimating odds ratios (OR) per standard deviation and 95% confidence intervals (CI). Results: HDL was positively associated with DLBCL (OR = 1.14; 95% CI, 1.00–1.30) and MZL (OR = 1.09; 95% CI, 1.01–1.18), while TG was inversely associated with MZL risk (OR = 0.90; 95% CI, 0.83–0.99), all at nominal significance (P < 0.05). A positive trend was observed for HDL with FL risk (OR = 1.08; 95% CI, 0.99–1.19; P = 0.087). No associations were noteworthy after adjusting for multiple testing. Conclusions: We did not find evidence of a clear or strong association of these lipid traits with the most common NHL subtypes. While these IVs have been previously linked to other cancers, our findings do not support any causal associations with these NHL subtypes. Impact: Our results suggest that prior reported inverse associations of lipid traits are not likely to be causal and could represent reverse causality or confounding.
Published: 2020

13. Inflammatory potential of diet and risk of lymphoma in the European Prospective Investigation into Cancer and Nutrition

Author: Solans, M. Benavente, Y. Saez, M. Agudo, A. Jakszyn, P. Naudin, S. Hosnijeh, F.S. Gunter, M. Huybrechts, I. Ferrari, P. Besson, C. Mahamat-Saleh, Y. Boutron-Ruault, M.-C. Kühn, T. Kaaks, R. Boeing, H. Lasheras, C. Sánchez, M.-J. Amiano, P. Chirlaque, M.D. Ardanaz, E. Schmidt, J.A. Vineis, P. Riboli, E. Trichopoulou, A. Karakatsani, A. Valanou, E. Masala, G. Agnoli, C. Tumino, R. Sacerdote, C. Mattiello, A. Skeie, G. Weiderpass, E. Jerkeman, M. Dias, J.A. Späth, F. Nilsson, L.M. Dahm, C.C. Overvad, K. Petersen, K.E.N. Tjønneland, A. de Sanjose, S. Vermeulen, R. Nieters, A. Casabonne, D.
Subjects: hemic and lymphatic diseases
Abstract: Introduction: Chronic inflammation plays a critical role in lymphomagenesis and several dietary factors seem to be involved its regulation. The aim of the current study was to assess the association between the inflammatory potential of the diet and the risk of lymphoma and its subtypes in the European Investigation into Cancer and Nutrition (EPIC) study. Methods: The analysis included 476,160 subjects with an average follow-up of 13.9 years, during which 3,136 lymphomas (135 Hodgkin lymphoma (HL), 2606 non-Hodgkin lymphoma (NHL) and 395 NOS) were identified. The dietary inflammatory potential was assessed by means of an inflammatory score of the diet (ISD), calculated using 28 dietary components and their corresponding inflammatory weights. The association between the ISD and lymphoma risk was estimated by hazard ratios (HR) and 95% confidence intervals (CI) calculated by multivariable Cox regression models adjusted for potential confounders. Results: The ISD was not associated with overall lymphoma risk. Among lymphoma subtypes, a positive association between the ISD and mature B-cell NHL (HR for a 1-SD increase: 1.07 (95% CI 1.01; 1.14), p trend = 0.03) was observed. No statistically significant association was found among other subtypes. However, albeit with smaller number of cases, a suggestive association was observed for HL (HR for a 1-SD increase = 1.22 (95% CI 0.94; 1.57), p trend 0.13). Conclusions: Our findings suggested that a high ISD score, reflecting a pro-inflammatory diet, was modestly positively associated with the risk of B-cell lymphoma subtypes. Further large prospective studies on low-grade inflammation induced by diet are warranted to confirm these findings. © 2019, Springer-Verlag GmbH Germany, part of Springer Nature.
Published: 2020

14. Genetically Determined Height and Risk of Non-hodgkin Lymphoma

Author: Moore, A., Kane, E., Panagiotou, O.A., Teras, L.R., Monnereau, A., Wong Doo, N., Machiela, M.J., Skibola, C.F., Slager, S.L., Salles, G., Camp, N.J., Bracci, P.M., Nieters, A., Vermeulen, R.C.H., Vijai, J., Smedby, K.E., Vajdic, C.M., Cozen, W., Spinelli, J.J., Hjalgrim, H., Giles, G.G., Link, B.K., Clavel, J., Arslan, A.A., Purdue, M.P., Tinker, L.F., Albanes, D., Ferri, G.M., Habermann, T.M., Adami, H.-O., Becker, N., Benavente, Y., Bisanzi, S., Boffetta, P., Brennan, P., Brooks-Wilson, A.R., Canzian, F., Conde, L., Cox, D.G., Curtin, K., Foretova, L., Gapstur, S.M., Ghesquières, H., Glenn, M., Glimelius, B., Jackson, R.D., Lan, Q., Liebow, M., Maynadie, M., McKay, J., Melbye, M., Miligi, L., Milne, R.L., Molina, T.J., Morton, L.M., North, K.E., Offit, K., Padoan, M., Piro, S., Ravichandran, V., Riboli, E., de Sanjose, S., Severson, R.K., Southey, M.C., Staines, A., Stewart, C., Travis, R.C., Weiderpass, E., Weinstein, S., Zheng, T., Chanock, S.J., Chatterjee, N., Rothman, N., Birmann, B.M., Cerhan, J.R., Berndt, S.I., IRAS OH Epidemiology Chemical Agents, and dIRAS RA-2
Subjects: follicular lymphoma, non-Hodgkin lymphoma, polygenic risk score, diffuse large B-celllymphoma, chronic lymphocytic leukemia, genetics, marginal zone lymphoma, height
Abstract: Although the evidence is not consistent, epidemiologic studies have suggested that taller adult height may be associated with an increased risk of some non-Hodgkin lymphoma (NHL) subtypes. Height is largely determined by genetic factors, but how these genetic factors may contribute to NHL risk is unknown. We investigated the relationship between genetic determinants of height and NHL risk using data from eight genome-wide association studies (GWAS) comprising 10,629 NHL cases, including 3,857 diffuse large B-cell lymphoma (DLBCL), 2,847 follicular lymphoma (FL), 3,100 chronic lymphocytic leukemia (CLL), and 825 marginal zone lymphoma (MZL) cases, and 9,505 controls of European ancestry. We evaluated genetically predicted height by constructing polygenic risk scores using 833 height-associated SNPs. We used logistic regression to estimate odds ratios (OR) and 95% confidence intervals (CI) for association between genetically determined height and the risk of four NHL subtypes in each GWAS and then used fixed-effect meta-analysis to combine subtype results across studies. We found suggestive evidence between taller genetically determined height and increased CLL risk (OR = 1.08, 95% CI = 1.00–1.17, p = 0.049), which was slightly stronger among women (OR = 1.15, 95% CI: 1.01–1.31, p = 0.036). No significant associations were observed with DLBCL, FL, or MZL. Our findings suggest that there may be some shared genetic factors between CLL and height, but other endogenous or environmental factors may underlie reported epidemiologic height associations with other subtypes.
Published: 2020

15. Serum levels of hsa-miR-16-5p, hsa-miR-29a-3p, hsa-miR-150-5p, hsa-miR-155-5p and hsa-miR-223-3p and subsequent risk of chronic lymphocytic leukemia in the EPIC study

Author: Casabonne, D. Benavente, Y. Seifert, J. Costas, L. Armesto, M. Arestin, M. Besson, C. Hosnijeh, F.S. Duell, E.J. Weiderpass, E. Masala, G. Kaaks, R. Canzian, F. Chirlaque, M.-D. Perduca, V. Mancini, F.R. Pala, V. Trichopoulou, A. Karakatsani, A. La Vecchia, C. Sánchez, M.-J. Tumino, R. Gunter, M.J. Amiano, P. Panico, S. Sacerdote, C. Schmidt, J.A. Boeing, H. Schulze, M.B. Barricarte, A. Riboli, E. Olsen, A. Tjønneland, A. Vermeulen, R. Nieters, A. Lawrie, C.H. de Sanjosé, S.
Subjects: body regions, embryonic structures
Abstract: Chronic lymphocytic leukemia (CLL) is an incurable disease accounting for almost one-third of leukemias in the Western world. Aberrant expression of microRNAs (miRNAs) is a well-established characteristic of CLL, and the robust nature of miRNAs makes them eminently suitable liquid biopsy biomarkers. Using a nested case–control study within the European Prospective Investigation into Cancer and Nutrition (EPIC), the predictive values of five promising human miRNAs (hsa-miR-16-5p, hsa-miR-29a-3p, hsa-miR-150-5p, hsa-miR-155-5p and hsa-miR-223-3p), identified in a pilot study, were examined in serum of 224 CLL cases (diagnosed 3 months to 18 years after enrollment) and 224 matched controls using Taqman based assays. Conditional logistic regressions were applied to adjust for potential confounders. The median time from blood collection to CLL diagnosis was 10 years (p25–p75: 7–13 years). Overall, the upregulation of hsa-miR-150-5p, hsa-miR-155-5p and hsa-miR-29a-3p was associated with subsequent risk of CLL [OR1∆Ct-unit increase (95%CI) = 1.42 (1.18–1.72), 1.64 (1.31–2.04) and 1.75 (1.31–2.34) for hsa-miR-150-5p, hsa-miR-155-5p and hsa-miR-29a-3p, respectively] and the strongest associations were observed within 10 years of diagnosis. However, the predictive performance of these miRNAs was modest (area under the curve
Published: 2020

16. Association between anthropometry and lifestyle factors and risk of B-cell lymphoma: An exposome-wide analysis

Author: Saberi Hosnijeh, F. (Fatemeh), Casabonne, D. (Delphine), Nieters, A. (Alexandra), Solans, M. (Marta), Naudin, S. (Sabine), Ferrari, P. (Pietro), Mckay, J.D. (James D.), Benavente, Y. (Yolanda), Weiderpass, E. (Elisabete), Freisling, H. (Heinz), Severi, G. (Gianluca), Boutron Ruault, M.-C. (Marie-Christine), Besson, C. (Caroline), Agnoli, C. (Claudia), Masala, G. (Giovanna), Sacerdote, C. (Carlotta), Tumino, R. (Rosario), Huerta, J.M. (José María), Amiano, P. (Pilar), Rodriguez-Barranco, M. (Miguel), Bonet, C. (Catalina), Barricarte, A. (Aurelio), Christakoudi, S. (Sofia), Knuppel, A. (Anika), Bueno-de-Mesquita, B. (Bas), Schulze, M.B. (Matthias), Kaaks, R. (Rudolf), Canzian, F. (Federico), Späth, F. (Florentin), Jerkeman, M. (Mats), Rylander, C. (Charlotta), Tjønneland, A. (Anne), Olsen, A. (Anja), Borch, K.B. (Kristin Benjaminsen), Vermeulen, R. (Roel), Saberi Hosnijeh, F. (Fatemeh), Casabonne, D. (Delphine), Nieters, A. (Alexandra), Solans, M. (Marta), Naudin, S. (Sabine), Ferrari, P. (Pietro), Mckay, J.D. (James D.), Benavente, Y. (Yolanda), Weiderpass, E. (Elisabete), Freisling, H. (Heinz), Severi, G. (Gianluca), Boutron Ruault, M.-C. (Marie-Christine), Besson, C. (Caroline), Agnoli, C. (Claudia), Masala, G. (Giovanna), Sacerdote, C. (Carlotta), Tumino, R. (Rosario), Huerta, J.M. (José María), Amiano, P. (Pilar), Rodriguez-Barranco, M. (Miguel), Bonet, C. (Catalina), Barricarte, A. (Aurelio), Christakoudi, S. (Sofia), Knuppel, A. (Anika), Bueno-de-Mesquita, B. (Bas), Schulze, M.B. (Matthias), Kaaks, R. (Rudolf), Canzian, F. (Federico), Späth, F. (Florentin), Jerkeman, M. (Mats), Rylander, C. (Charlotta), Tjønneland, A. (Anne), Olsen, A. (Anja), Borch, K.B. (Kristin Benjaminsen), and Vermeulen, R. (Roel)
Abstract: To better understand the role of individual and lifestyle factors in human disease, an exposome-wide association study was performed to investigate within a single-study anthropometry measures and lifestyle factors previously associated with B-cell lymphoma (BCL). Within the European Prospective Investigation into Cancer and nutrition study, 2402 incident BCL cases were diagnosed from 475 426 participants that were followed-up on average 14 years. Standard and penalized Cox regression models as well as principal component analysis (PCA) were used to evaluate 84 exposures in relation to BCL risk. Standard and penalized Cox regression models showed a positive association between anthropometric measures and BCL and multiple myeloma/plasma cell neoplasm (MM). The penalized Cox models additionally showed the association between several exposures from categories of physical activity, smoking status, medical history, socioeconomic position, diet and BCL and/or the subtypes. PCAs confirmed the individual a
Published: 2020
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17. Genetically Determined Height and Risk of Non-hodgkin Lymphoma

Author: IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Moore, A., Kane, E., Panagiotou, O.A., Teras, L.R., Monnereau, A., Wong Doo, N., Machiela, M.J., Skibola, C.F., Slager, S.L., Salles, G., Camp, N.J., Bracci, P.M., Nieters, A., Vermeulen, R.C.H., Vijai, J., Smedby, K.E., Vajdic, C.M., Cozen, W., Spinelli, J.J., Hjalgrim, H., Giles, G.G., Link, B.K., Clavel, J., Arslan, A.A., Purdue, M.P., Tinker, L.F., Albanes, D., Ferri, G.M., Habermann, T.M., Adami, H.-O., Becker, N., Benavente, Y., Bisanzi, S., Boffetta, P., Brennan, P., Brooks-Wilson, A.R., Canzian, F., Conde, L., Cox, D.G., Curtin, K., Foretova, L., Gapstur, S.M., Ghesquières, H., Glenn, M., Glimelius, B., Jackson, R.D., Lan, Q., Liebow, M., Maynadie, M., McKay, J., Melbye, M., Miligi, L., Milne, R.L., Molina, T.J., Morton, L.M., North, K.E., Offit, K., Padoan, M., Piro, S., Ravichandran, V., Riboli, E., de Sanjose, S., Severson, R.K., Southey, M.C., Staines, A., Stewart, C., Travis, R.C., Weiderpass, E., Weinstein, S., Zheng, T., Chanock, S.J., Chatterjee, N., Rothman, N., Birmann, B.M., Cerhan, J.R., Berndt, S.I., IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Moore, A., Kane, E., Panagiotou, O.A., Teras, L.R., Monnereau, A., Wong Doo, N., Machiela, M.J., Skibola, C.F., Slager, S.L., Salles, G., Camp, N.J., Bracci, P.M., Nieters, A., Vermeulen, R.C.H., Vijai, J., Smedby, K.E., Vajdic, C.M., Cozen, W., Spinelli, J.J., Hjalgrim, H., Giles, G.G., Link, B.K., Clavel, J., Arslan, A.A., Purdue, M.P., Tinker, L.F., Albanes, D., Ferri, G.M., Habermann, T.M., Adami, H.-O., Becker, N., Benavente, Y., Bisanzi, S., Boffetta, P., Brennan, P., Brooks-Wilson, A.R., Canzian, F., Conde, L., Cox, D.G., Curtin, K., Foretova, L., Gapstur, S.M., Ghesquières, H., Glenn, M., Glimelius, B., Jackson, R.D., Lan, Q., Liebow, M., Maynadie, M., McKay, J., Melbye, M., Miligi, L., Milne, R.L., Molina, T.J., Morton, L.M., North, K.E., Offit, K., Padoan, M., Piro, S., Ravichandran, V., Riboli, E., de Sanjose, S., Severson, R.K., Southey, M.C., Staines, A., Stewart, C., Travis, R.C., Weiderpass, E., Weinstein, S., Zheng, T., Chanock, S.J., Chatterjee, N., Rothman, N., Birmann, B.M., Cerhan, J.R., and Berndt, S.I.
Published: 2020

18. Lipid trait variants and the risk of non-hodgkin lymphoma subtypes: a mendelian randomization study

Author: IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Kleinstern, G., Camp, N.J., Berndt, S.I., Birmann, B.M., Nieters, A., Bracci, P.M., McKay, J.D., Ghesquieres, H., Lan, Q., Hjalgrim, H., Benavente, Y., Monnereau, A., Purdue, M.P., Zeleniuch-Jacquotte, A., Giles, G.G., Vermeulen, R., Cocco, P., Albanes, D., Teras, L.R., Brooks-Wilson, A.R., Vajdic, C.M., Kane, E., Caporaso, N.E., Smedby, K.E., Salles, G., Vijai, J., Chanock, S.J., Skibola, C.F., Rothman, N., Slager, S.L., Cerhan, J.R., IRAS OH Epidemiology Chemical Agents, dIRAS RA-2, Kleinstern, G., Camp, N.J., Berndt, S.I., Birmann, B.M., Nieters, A., Bracci, P.M., McKay, J.D., Ghesquieres, H., Lan, Q., Hjalgrim, H., Benavente, Y., Monnereau, A., Purdue, M.P., Zeleniuch-Jacquotte, A., Giles, G.G., Vermeulen, R., Cocco, P., Albanes, D., Teras, L.R., Brooks-Wilson, A.R., Vajdic, C.M., Kane, E., Caporaso, N.E., Smedby, K.E., Salles, G., Vijai, J., Chanock, S.J., Skibola, C.F., Rothman, N., Slager, S.L., and Cerhan, J.R.
Published: 2020

19. Genetically Determined Height and Risk of Non-hodgkin Lymphoma

Author: Moore, A, Kane, E, Wang, Z, Panagiotou, OA, Teras, LR, Monnereau, A, Wong Doo, N, Machiela, MJ, Skibola, CF, Slager, SL, Salles, G, Camp, NJ, Bracci, PM, Nieters, A, Vermeulen, RCH, Vijai, J, Smedby, KE, Zhang, Y, Vajdic, CM, Cozen, W, Spinelli, JJ, Hjalgrim, H, Giles, GG, Link, BK, Clavel, J, Arslan, AA, Purdue, MP, Tinker, LF, Albanes, D, Ferri, GM, Habermann, TM, Adami, H-O, Becker, N, Benavente, Y, Bisanzi, S, Boffetta, P, Brennan, P, Brooks-Wilson, AR, Canzian, F, Conde, L, Cox, DG, Curtin, K, Foretova, L, Gapstur, SM, Ghesquieres, H, Glenn, M, Glimelius, B, Jackson, RD, Lan, Q, Liebow, M, Maynadie, M, McKay, J, Melbye, M, Miligi, L, Milne, RL, Molina, TJ, Morton, LM, North, KE, Offit, K, Padoan, M, Patel, AV, Piro, S, Ravichandran, V, Riboli, E, de Sanjose, S, Severson, RK, Southey, MC, Staines, A, Stewart, C, Travis, RC, Weiderpass, E, Weinstein, S, Zheng, T, Chanock, SJ, Chatterjee, N, Rothman, N, Birmann, BM, Cerhan, JR, Berndt, SI, Moore, A, Kane, E, Wang, Z, Panagiotou, OA, Teras, LR, Monnereau, A, Wong Doo, N, Machiela, MJ, Skibola, CF, Slager, SL, Salles, G, Camp, NJ, Bracci, PM, Nieters, A, Vermeulen, RCH, Vijai, J, Smedby, KE, Zhang, Y, Vajdic, CM, Cozen, W, Spinelli, JJ, Hjalgrim, H, Giles, GG, Link, BK, Clavel, J, Arslan, AA, Purdue, MP, Tinker, LF, Albanes, D, Ferri, GM, Habermann, TM, Adami, H-O, Becker, N, Benavente, Y, Bisanzi, S, Boffetta, P, Brennan, P, Brooks-Wilson, AR, Canzian, F, Conde, L, Cox, DG, Curtin, K, Foretova, L, Gapstur, SM, Ghesquieres, H, Glenn, M, Glimelius, B, Jackson, RD, Lan, Q, Liebow, M, Maynadie, M, McKay, J, Melbye, M, Miligi, L, Milne, RL, Molina, TJ, Morton, LM, North, KE, Offit, K, Padoan, M, Patel, AV, Piro, S, Ravichandran, V, Riboli, E, de Sanjose, S, Severson, RK, Southey, MC, Staines, A, Stewart, C, Travis, RC, Weiderpass, E, Weinstein, S, Zheng, T, Chanock, SJ, Chatterjee, N, Rothman, N, Birmann, BM, Cerhan, JR, and Berndt, SI
Abstract: Although the evidence is not consistent, epidemiologic studies have suggested that taller adult height may be associated with an increased risk of some non-Hodgkin lymphoma (NHL) subtypes. Height is largely determined by genetic factors, but how these genetic factors may contribute to NHL risk is unknown. We investigated the relationship between genetic determinants of height and NHL risk using data from eight genome-wide association studies (GWAS) comprising 10,629 NHL cases, including 3,857 diffuse large B-cell lymphoma (DLBCL), 2,847 follicular lymphoma (FL), 3,100 chronic lymphocytic leukemia (CLL), and 825 marginal zone lymphoma (MZL) cases, and 9,505 controls of European ancestry. We evaluated genetically predicted height by constructing polygenic risk scores using 833 height-associated SNPs. We used logistic regression to estimate odds ratios (OR) and 95% confidence intervals (CI) for association between genetically determined height and the risk of four NHL subtypes in each GWAS and then used fixed-effect meta-analysis to combine subtype results across studies. We found suggestive evidence between taller genetically determined height and increased CLL risk (OR = 1.08, 95% CI = 1.00-1.17, p = 0.049), which was slightly stronger among women (OR = 1.15, 95% CI: 1.01-1.31, p = 0.036). No significant associations were observed with DLBCL, FL, or MZL. Our findings suggest that there may be some shared genetic factors between CLL and height, but other endogenous or environmental factors may underlie reported epidemiologic height associations with other subtypes.
Published: 2020

20. Occupational heat exposure and breast cancer risk (MCC-Spain study)

Author: Hinchliffe, A., primary, Kogevinas, M., additional, Castano-Vinyals, G., additional, Marcos-Delgado, A., additional, Pollan, M., additional, Fernandez-Tardon, G., additional, Perez-Gomez, B., additional, Amiano, P., additional, Moreno, V., additional, Alguacil, J., additional, Marcos-Gragera, R., additional, Ardanaz, E., additional, Aragones, N., additional, Benavente, Y., additional, Salas, D., additional, Llorca, J., additional, and Turner, M.C., additional
Published: 2020
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21. DESIGUALDADES DE GÉNERO, EDAD Y SITUACIÓN SOCIOLABORAL. PROGRAMA DE ACTIVIDAD FÍSICA ACTIVA-MURCIA

Author: López-Benavente, Y., primary, Abad-Corpa, E., additional, Lidón-Cerezuela, M.B., additional, Vivo-Molina, M.C., additional, Menárguez-Puche, J.F., additional, Ros-Sánchez, T., additional, and Meseguer-Liza, C., additional
Published: 2020
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22. Reproductive Factors, Exogenous Hormone Use, and Risk of B-Cell Non-Hodgkin Lymphoma in a Cohort of Women from the European Prospective Investigation into Cancer and Nutrition

Author: Costas, L. Lujan-Barroso, L. Benavente, Y. Allen, N.E. Amiano, P. Ardanaz, E. Besson, C. Boeing, H. Bueno-De-Mesquita, B. Cervenka, I. Fortner, R.T. Fournier, A. Gunter, M. Harlid, S. Huerta, J.M. Jerkeman, M. Jirström, K. Kaaks, R. Karakatsani, A. Khaw, K.-T. Kotanidou, A. Lund, E. Masala, G. Mattiello, A. Melin, B. Menéndez, V. Murphy, N. Nieters, A. Overvad, K. Riboli, E. Sacerdote, C. Sánchez, M.-J. Schmidt, J.A. Sieri, S. Tjønneland, A. Trichopoulou, A. Tumino, R. Vermeulen, R. Weiderpass, E. De Sanjosé, S. Agudo, A. Casabonne, D.
Abstract: The role of hormonal factors in the etiology of lymphoid neoplasms remains unclear. Previous studies have yielded conflicting results, have lacked sufficient statistical power to assess many lymphoma subtypes, or have lacked detailed information on relevant exposures. Within the European Prospective Investigation Into Cancer and Nutrition cohort, we analyzed comprehensive data on reproductive factors and exogenous hormone use collected at baseline (1992-2000) among 343,458 women, including data on 1,427 incident cases of B-cell non-Hodgkin lymphoma (NHL) and its major subtypes identified after a mean follow-up period of 14 years (through 2015). We estimated hazard ratios and 95% confidence intervals using multivariable proportional hazards modeling. Overall, we observed no statistically significant associations between parity, age at first birth, breastfeeding, oral contraceptive use, or ever use of postmenopausal hormone therapy and risk of B-cell NHL or its subtypes. Women who had undergone surgical menopause had a 51% higher risk of B-cell NHL (based on 67 cases) than women with natural menopause (hazard ratio = 1.51, 95% confidence interval: 1.17, 1.94). Given that this result may have been due to chance, our results provide little support for the hypothesis that sex hormones play a role in lymphomagenesis. © The Author(s) 2018.
Published: 2019

23. Adherence to the mediterranean diet and lymphoma risk in the european prospective investigation into cancer and nutrition

Author: Solans, M. Benavente, Y. Saez, M. Agudo, A. Naudin, S. Hosnijeh, F.S. Noh, H. Freisling, H. Ferrari, P. Besson, C. Mahamat-Saleh, Y. Boutron-Ruault, M.-C. Kühn, T. Kaaks, R. Boeing, H. Lasheras, C. Rodríguez-Barranco, M. Amiano, P. Huerta, J.M. Barricarte, A. Schmidt, J.A. Vineis, P. Riboli, E. Trichopoulou, A. Bamia, C. Peppa, E. Masala, G. Agnoli, C. Tumino, R. Sacerdote, C. Panico, S. Skeie, G. Weiderpass, E. Jerkeman, M. Ericson, U. Späth, F. Nilsson, L.M. Dahm, C.C. Overvad, K. Bolvig, A.K. Tjønneland, A. de Sanjose, S. Buckland, G. Vermeulen, R. Nieters, A. Casabonne, D.
Abstract: There is a growing evidence of the protective role of the Mediterranean diet (MD) on cancer. However, no prospective study has yet investigated its influence on lymphoma. We evaluated the association between adherence to the MD and risk of lymphoma and its subtypes in the European Prospective Investigation into Cancer and Nutrition (EPIC) study. The analysis included 476,160 participants, recruited from 10 European countries between 1991 and 2001. Adherence to the MD was estimated through the adapted relative MD (arMED) score excluding alcohol. Cox proportional hazards regression models were used while adjusting for potential confounders. During an average follow-up of 13.9 years, 3,136 lymphomas (135 Hodgkin lymphoma [HL], 2,606 non-HL and 395 lymphoma not otherwise specified) were identified. Overall, a 1-unit increase in the arMED score was associated with a 2% lower risk of lymphoma (95% CI: 0.97; 1.00, p-trend = 0.03) while a statistically nonsignificant inverse association between a high versus low arMED score and risk of lymphoma was observed (hazard ratio [HR]: 0.91 [95% CI 0.80; 1.03], p-trend = 0.12). Analyses by lymphoma subtype did not reveal any statistically significant associations. Albeit with small numbers of cases (N = 135), a suggestive inverse association was found for HL (HR 1-unit increase = 0.93 [95% CI: 0.86; 1.01], p-trend = 0.07). However, the study may have lacked statistical power to detect small effect sizes for lymphoma subtype. Our findings suggest that an increasing arMED score was inversely related to the risk of overall lymphoma in EPIC but not by subtypes. Further large prospective studies are warranted to confirm these findings. © 2018 UICC
Published: 2019

24. 1. Virology, Epidemiology: 003 THE EFFECT OF REGULAR USE OF HAIR DYE ON LYMPHOID NEOPLASM IN EUROPE

Author: de Sanjose, S., Benavente, Y., Nieters, A., Foretova, L., Maynadie, M., Cocco, P., Staines, A., Vornanen, M., Boffetta, P., Becker, N., Alvaro, T., and Brennan, P.
Published: 2005

25. Genetic overlap between autoimmune diseases and non-Hodgkin lymphoma subtypes

Author: Din, L., Sheikh, M., Kosaraju, N., Smedby, K.E., Bernatsky, S., Berndt, S.I., Skibola, C.F., Nieters, A., McKay, J.D., Cocco, P., Maynadié, M., Foretová, L., Staines, A., Mack, T.M., de Sanjosé, S., Vyse, T.J., Padyukov, L., Monnereau, A., Arslan, A.A., Moore, A., Brooks-Wilson, A.R., Glimelius, B., Birmann, B.M., Link, B.K., Stewart, C., Vajdic, C.M., Haioun, C., Magnani, C., Conti, D.V., Cox, D.G., Casabonne, D., Albanes, D., Kane, E., Roman, E., Muzi, G., Salles, G., Giles, G.G., Adami, H.-O., Ghesquières, H., De Vivo, I., Clavel, J., Cerhan, J.R., Spinelli, J.J., Vijai, J., Curtin, K., Costenbader, K.H., Onel, K., Offit, K., Teras, L.R., Morton, L., Conde, L., Miligi, L., Melbye, M., Ennas, M.G., Liebow, M., Purdue, M.P., Glenn, M., Southey, M.C., Din, M., Rothman, N., Camp, N.J., Wong Doo, N., Becker, N., Pradhan, N., Bracci, P.M., Boffetta, P., Vineis, P., Brennan, P., Kraft, P., Lan, Q., Severson, R.K., Vermeulen, R.C.H., Milne, R.L., Kaaks, R., Travis, R.C., Weinstein, S.J., Chanock, S.J., Ansell, S.M., Slager, S.L., Zheng, T., Benavente, Y., Taub, Z., Madireddy, L., Gourraud, P.-A., Oksenberg, J.R., Cozen, W., Hjalgrim, H., Khankhanian, P., Din, L., Sheikh, M., Kosaraju, N., Smedby, K.E., Bernatsky, S., Berndt, S.I., Skibola, C.F., Nieters, A., McKay, J.D., Cocco, P., Maynadié, M., Foretová, L., Staines, A., Mack, T.M., de Sanjosé, S., Vyse, T.J., Padyukov, L., Monnereau, A., Arslan, A.A., Moore, A., Brooks-Wilson, A.R., Glimelius, B., Birmann, B.M., Link, B.K., Stewart, C., Vajdic, C.M., Haioun, C., Magnani, C., Conti, D.V., Cox, D.G., Casabonne, D., Albanes, D., Kane, E., Roman, E., Muzi, G., Salles, G., Giles, G.G., Adami, H.-O., Ghesquières, H., De Vivo, I., Clavel, J., Cerhan, J.R., Spinelli, J.J., Vijai, J., Curtin, K., Costenbader, K.H., Onel, K., Offit, K., Teras, L.R., Morton, L., Conde, L., Miligi, L., Melbye, M., Ennas, M.G., Liebow, M., Purdue, M.P., Glenn, M., Southey, M.C., Din, M., Rothman, N., Camp, N.J., Wong Doo, N., Becker, N., Pradhan, N., Bracci, P.M., Boffetta, P., Vineis, P., Brennan, P., Kraft, P., Lan, Q., Severson, R.K., Vermeulen, R.C.H., Milne, R.L., Kaaks, R., Travis, R.C., Weinstein, S.J., Chanock, S.J., Ansell, S.M., Slager, S.L., Zheng, T., Benavente, Y., Taub, Z., Madireddy, L., Gourraud, P.-A., Oksenberg, J.R., Cozen, W., Hjalgrim, H., and Khankhanian, P.
Abstract: Epidemiologic studies show an increased risk of non-Hodgkin lymphoma (NHL) in patients with autoimmune disease (AD), due to a combination of shared environmental factors and/or genetic factors, or a causative cascade: chronic inflammation/antigen-stimulation in one disease leads to another. Here we assess shared genetic risk in genome-wide-association-studies (GWAS). Secondary analysis of GWAS of NHL subtypes (chronic lymphocytic leukemia, diffuse large B-cell lymphoma, follicular lymphoma, and marginal zone lymphoma) and ADs (rheumatoid arthritis, systemic lupus erythematosus, and multiple sclerosis). Shared genetic risk was assessed by (a) description of regional genetic of overlap, (b) polygenic risk score (PRS), (c)"diseasome", (d)meta-analysis. Descriptive analysis revealed few shared genetic factors between each AD and each NHL subtype. The PRS of ADs were not increased in NHL patients (nor vice versa). In the diseasome, NHLs shared more genetic etiology with ADs than solid cancers (p = .0041). A meta-analysis (combing AD with NHL) implicated genes of apoptosis and telomere length. This GWAS-based analysis four NHL subtypes and three ADs revealed few weakly-associated shared loci, explaining little total risk. This suggests common genetic variation, as assessed by GWAS in these sample sizes, may not be the primary explanation for the link between these ADs and NHLs.
Published: 2019

26. Genetic overlap between autoimmune diseases and non-Hodgkin lymphoma subtypes

Author: Din, L, Sheikh, M, Kosaraju, N, Smedby, KE, Bernatsky, S, Berndt, S, Skibola, CF, Nieters, A, Wang, S, McKay, JD, Cocco, P, Maynadie, M, Foretova, L, Staines, A, Mack, TM, de Sanjose, S, Vyse, TJ, Padyukov, L, Monnereau, A, Arslan, AA, Moore, A, Brooks-Wilson, AR, Novak, AJ, Glimelius, B, Birmann, BM, Link, BK, Stewart, C, Vajdic, CM, Haioun, C, Magnani, C, Conti, D, Cox, DG, Casabonne, D, Albanes, D, Kane, E, Roman, E, Muzi, G, Salles, G, Giles, GG, Adami, H-O, Ghesquieres, H, De Vivo, I, Clavel, J, Cerhan, JR, Spinelli, JJ, Hofmann, J, Vijai, J, Curtin, K, Costenbader, KH, Onel, K, Offit, K, Teras, LR, Morton, L, Conde, L, Miligi, L, Melbye, M, Ennas, MG, Liebow, M, Purdue, MP, Glenn, M, Southey, MC, Din, M, Rothman, N, Camp, NJ, Doo, NW, Becker, N, Pradhan, N, Bracci, PM, Boffetta, P, Vineis, P, Brennan, P, Kraft, P, Lan, Q, Severson, RK, Vermeulen, RCH, Milne, RL, Kaaks, R, Travis, RC, Weinstein, SJ, Chanock, SJ, Ansell, SM, Slager, SL, Zheng, T, Zhang, Y, Benavente, Y, Taub, Z, Madireddy, L, Gourraud, P-A, Oksenberg, JR, Cozen, W, Hjalgrim, H, Khankhanian, P, Din, L, Sheikh, M, Kosaraju, N, Smedby, KE, Bernatsky, S, Berndt, S, Skibola, CF, Nieters, A, Wang, S, McKay, JD, Cocco, P, Maynadie, M, Foretova, L, Staines, A, Mack, TM, de Sanjose, S, Vyse, TJ, Padyukov, L, Monnereau, A, Arslan, AA, Moore, A, Brooks-Wilson, AR, Novak, AJ, Glimelius, B, Birmann, BM, Link, BK, Stewart, C, Vajdic, CM, Haioun, C, Magnani, C, Conti, D, Cox, DG, Casabonne, D, Albanes, D, Kane, E, Roman, E, Muzi, G, Salles, G, Giles, GG, Adami, H-O, Ghesquieres, H, De Vivo, I, Clavel, J, Cerhan, JR, Spinelli, JJ, Hofmann, J, Vijai, J, Curtin, K, Costenbader, KH, Onel, K, Offit, K, Teras, LR, Morton, L, Conde, L, Miligi, L, Melbye, M, Ennas, MG, Liebow, M, Purdue, MP, Glenn, M, Southey, MC, Din, M, Rothman, N, Camp, NJ, Doo, NW, Becker, N, Pradhan, N, Bracci, PM, Boffetta, P, Vineis, P, Brennan, P, Kraft, P, Lan, Q, Severson, RK, Vermeulen, RCH, Milne, RL, Kaaks, R, Travis, RC, Weinstein, SJ, Chanock, SJ, Ansell, SM, Slager, SL, Zheng, T, Zhang, Y, Benavente, Y, Taub, Z, Madireddy, L, Gourraud, P-A, Oksenberg, JR, Cozen, W, Hjalgrim, H, and Khankhanian, P
Abstract: Epidemiologic studies show an increased risk of non-Hodgkin lymphoma (NHL) in patients with autoimmune disease (AD), due to a combination of shared environmental factors and/or genetic factors, or a causative cascade: chronic inflammation/antigen-stimulation in one disease leads to another. Here we assess shared genetic risk in genome-wide-association-studies (GWAS). Secondary analysis of GWAS of NHL subtypes (chronic lymphocytic leukemia, diffuse large B-cell lymphoma, follicular lymphoma, and marginal zone lymphoma) and ADs (rheumatoid arthritis, systemic lupus erythematosus, and multiple sclerosis). Shared genetic risk was assessed by (a) description of regional genetic of overlap, (b) polygenic risk score (PRS), (c)"diseasome", (d)meta-analysis. Descriptive analysis revealed few shared genetic factors between each AD and each NHL subtype. The PRS of ADs were not increased in NHL patients (nor vice versa). In the diseasome, NHLs shared more genetic etiology with ADs than solid cancers (p = .0041). A meta-analysis (combing AD with NHL) implicated genes of apoptosis and telomere length. This GWAS-based analysis four NHL subtypes and three ADs revealed few weakly-associated shared loci, explaining little total risk. This suggests common genetic variation, as assessed by GWAS in these sample sizes, may not be the primary explanation for the link between these ADs and NHLs.
Published: 2019

27. Genome-wide association analysis implicates dysregulation of immunity genes in chronic lymphocytic leukemia

Author: Law, PJ, Berndt, SI, Speedy, HE, Camp, NJ, Sava, GP, Skibola, CF, Holroyd, A, Joseph, V, Sunter, NJ, Nieters, A, Bea, S, Monnereau, A, Martin-Garcia, D, Goldin, LR, Clot, G, Teras, LR, Quintela, I, Birmann, BM, Jayne, S, Cozen, W, Majid, A, Smedby, KE, Dearden, C, Brooks-Wilson, AR, Hall, AG, Purdue, MP, Mainou-Fowler, T, Vajdic, CM, Jackson, GH, Cocco, P, Marr, H, Zhang, Y, Zheng, T, Giles, GG, Lawrence, C, Call, TG, Liebow, M, Melbye, M, Glimelius, B, Mansouri, L, Glenn, M, Curtin, K, Diver, WR, Link, BK, Conde, L, Bracci, PM, Holly, EA, Jackson, RD, Tinker, LF, Benavente, Y, Boffetta, P, Brennan, P, Maynadie, M, McKay, J, Albanes, D, Weinstein, S, Wang, Z, Caporaso, NE, Morton, LM, Severson, RK, Riboli, E, Vineis, P, Vermeulen, RCH, Southey, MC, Milne, RL, Clavel, J, Topka, S, Spinelli, JJ, Kraft, P, Grazia Ennas, M, Summerfield, G, Ferri, GM, Harris, RJ, Miligi, L, Pettitt, AR, North, KE, Allsup, DJ, Fraumeni, JF, Bailey, JR, Offit, K, Pratt, G, Hjalgrim, H, Pepper, C, Chanock, SJ, Fegan, C, Rosenquist, R, De Sanjose, S, Carracedo, A, Dyer, MJS, Catovsky, D, Campo, E, Cerhan, JR, Allan, JM, Rothman, N, Houlston, R, and Slager, S
Subjects: RISK, CHROMATIN, Science & Technology, LOCI, VARIANTS, DISEASE, Multidisciplinary Sciences, TRANSCRIPTION FACTORS, MD Multidisciplinary, IMPUTATION, Science & Technology - Other Topics, BREAST-CANCER, COMMON VARIATION, METAANALYSIS
Abstract: Several chronic lymphocytic leukemia (CLL) susceptibility loci have been reported, however much of the heritable risk remains unidentified. Here we perform a meta-analysis of six genome-wide association studies, imputed using a merged reference panel of 1000 Genomes and UK10K data, totaling 6,200 cases and 17,598 controls after replication. We identify nine risk loci at 1p36.11 (rs34676223, P = 5.04x10-13), 1q42.13 (rs41271473, P = 1.06x10-10), 4q24 (rs71597109, P = 1.37x10-10), 4q35.1 (rs57214277, P = 3.69x10-8), 6p21.31 (rs3800461, P = 1.97x10-8), 11q23.2 (rs61904987, P = 2.64x10-11), 18q21.1 (rs1036935, P = 3.27x10-8), 19p13.3 (rs7254272, P = 4.67x10-8) and 22q13.33 (rs140522, P = 2.70x10-9). These new and established risk loci map to areas of active chromatin and show an over-representation of transcription factor binding for key determinants of B-cell development and immune response.
Published: 2016

28. GENDER, AGE AND SOCIO-OCCUPATIONAL INEQUALITIES. ACTIVA-MURCIA PHYSICAL ACTIVITY PROGRAM.

Author: López-Benavente, Y., Abad-Corpa, E., Lidón-Cerezuela, M. B., Vivo-Molina, M. C., Menárguez-Puche, J. F., Ros-Sánchez, T., and Meseguer-Liza, C.
Subjects: PHYSICAL activity, GENDER inequality
Abstract: Copyright of International Journal of Medicine & Science of Physical Activity & Sport / Revista Internacional de Medicina y Ciencias de la Actividad Física y del Deporte is the property of Revista Internacional de Medicina y Ciencias de la Actividad Fisica y del Deporte and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Published: 2020
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29. Compositional analysis of dietary patterns

Author: Solans, M, primary, Coenders, G, additional, Marcos-Gragera, R, additional, Castelló, A, additional, Gràcia-Lavedan, E, additional, Benavente, Y, additional, Moreno, V, additional, Pérez-Gómez, B, additional, Amiano, P, additional, Fernández-Villa, T, additional, Guevara, M, additional, Gómez-Acebo, I, additional, Fernández-Tardón, G, additional, Vanaclocha-Espi, M, additional, Chirlaque, MD, additional, Capelo, R, additional, Barrios, R, additional, Aragonés, N, additional, Molinuevo, A, additional, Vitelli-Storelli, F, additional, Castilla, J, additional, Dierssen-Sotos, T, additional, Castaño-Vinyals, G, additional, Kogevinas, M, additional, Pollán, M, additional, and Saez, M, additional
Published: 2018
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30. Genome-wide association analysis implicates dysregulation of immunity genes in chronic lymphocytic leukaemia

Author: Law, PJ, Berndt, SI, Speedy, HE, Camp, NJ, Sava, GP, Skibola, CF, Holroyd, A, Joseph, V, Sunter, NJ, Nieters, A, Bea, S, Monnereau, A, Martin-Garcia, D, Goldin, LR, Clot, G, Teras, LR, Quintela, I, Birmann, BM, Jayne, S, Cozen, W, Majid, A, Smedby, KE, Lan, Q, Dearden, C, Brooks-Wilson, AR, Hall, AG, Purdue, MP, Mainou-Fowler, T, Vajdic, CM, Jackson, GH, Cocco, P, Marr, H, Zhang, Y, Zheng, T, Giles, GG, Lawrence, C, Call, TG, Liebow, M, Melbye, M, Glimelius, B, Mansouri, L, Glenn, M, Curtin, K, Diver, WR, Link, BK, Conde, L, Bracci, PM, Holly, EA, Jackson, RD, Tinker, LF, Benavente, Y, Boffetta, P, Brennan, P, Maynadie, M, McKay, J, Albanes, D, Weinstein, S, Wang, Z, Caporaso, NE, Morton, LM, Severson, RK, Riboli, E, Vineis, P, Vermeulen, RCH, Southey, MC, Milne, RL, Clavel, J, Topka, S, Spinelli, JJ, Kraft, P, Ennas, MG, Summerfield, G, Ferri, GM, Harris, RJ, Miligi, L, Pettitt, AR, North, KE, Allsup, DJ, Fraumeni, JF, Bailey, JR, Offit, K, Pratt, G, Hjalgrim, H, Pepper, C, Chanock, SJ, Fegan, C, Rosenquist, R, de Sanjose, S, Carracedo, A, Dyer, MJS, Catovsky, D, Campo, E, Cerhan, JR, Allan, JM, Rothman, N, Houlston, R, Slager, SL, Law, PJ, Berndt, SI, Speedy, HE, Camp, NJ, Sava, GP, Skibola, CF, Holroyd, A, Joseph, V, Sunter, NJ, Nieters, A, Bea, S, Monnereau, A, Martin-Garcia, D, Goldin, LR, Clot, G, Teras, LR, Quintela, I, Birmann, BM, Jayne, S, Cozen, W, Majid, A, Smedby, KE, Lan, Q, Dearden, C, Brooks-Wilson, AR, Hall, AG, Purdue, MP, Mainou-Fowler, T, Vajdic, CM, Jackson, GH, Cocco, P, Marr, H, Zhang, Y, Zheng, T, Giles, GG, Lawrence, C, Call, TG, Liebow, M, Melbye, M, Glimelius, B, Mansouri, L, Glenn, M, Curtin, K, Diver, WR, Link, BK, Conde, L, Bracci, PM, Holly, EA, Jackson, RD, Tinker, LF, Benavente, Y, Boffetta, P, Brennan, P, Maynadie, M, McKay, J, Albanes, D, Weinstein, S, Wang, Z, Caporaso, NE, Morton, LM, Severson, RK, Riboli, E, Vineis, P, Vermeulen, RCH, Southey, MC, Milne, RL, Clavel, J, Topka, S, Spinelli, JJ, Kraft, P, Ennas, MG, Summerfield, G, Ferri, GM, Harris, RJ, Miligi, L, Pettitt, AR, North, KE, Allsup, DJ, Fraumeni, JF, Bailey, JR, Offit, K, Pratt, G, Hjalgrim, H, Pepper, C, Chanock, SJ, Fegan, C, Rosenquist, R, de Sanjose, S, Carracedo, A, Dyer, MJS, Catovsky, D, Campo, E, Cerhan, JR, Allan, JM, Rothman, N, Houlston, R, and Slager, SL
Abstract: Several chronic lymphocytic leukaemia (CLL) susceptibility loci have been reported; however, much of the heritable risk remains unidentified. Here we perform a meta-analysis of six genome-wide association studies, imputed using a merged reference panel of 1,000 Genomes and UK10K data, totalling 6,200 cases and 17,598 controls after replication. We identify nine risk loci at 1p36.11 (rs34676223, P=5.04 × 10-13), 1q42.13 (rs41271473, P=1.06 × 10-10), 4q24 (rs71597109, P=1.37 × 10-10), 4q35.1 (rs57214277, P=3.69 × 10-8), 6p21.31 (rs3800461, P=1.97 × 10-8), 11q23.2 (rs61904987, P=2.64 × 10-11), 18q21.1 (rs1036935, P=3.27 × 10-8), 19p13.3 (rs7254272, P=4.67 × 10-8) and 22q13.33 (rs140522, P=2.70 × 10-9). These new and established risk loci map to areas of active chromatin and show an over-representation of transcription factor binding for the key determinants of B-cell development and immune response.
Published: 2017

31. Lupus-related single nucleotide polymorphisms and risk of diffuse large B-cell lymphoma

Author: Bernatsky, S, Garcia, HAV, Spinelli, JJ, Gaffney, P, Smedby, KE, Ramsey-Goldman, R, Wang, SS, Adami, H-O, Albanes, D, Angelucci, E, Ansell, SM, Asmann, YW, Becker, N, Benavente, Y, Berndt, SI, Bertrand, KA, Birmann, BM, Boeing, H, Boffetta, P, Bracci, PM, Brennan, P, Brooks-Wilson, AR, Cerhan, JR, Chanock, SJ, Clavel, J, Conde, L, Cotenbader, KH, Cox, DG, Cozen, W, Crouch, S, De Roos, AJ, de Sanjose, S, Di Lollo, S, Diver, WR, Dogan, A, Foretova, L, Ghesquieres, H, Giles, GG, Glimelius, B, Habermann, TM, Haioun, C, Hartge, P, Hjalgrim, H, Holford, TR, Holly, EA, Jackson, RD, Kaaks, R, Kane, E, Kelly, RS, Klein, RJ, Kraft, P, Kricker, A, Lan, Q, Lawrence, C, Liebow, M, Lightfoot, T, Link, BK, Maynadie, M, Mckay, J, Melbye, M, Molina, TJ, Monnereau, A, Morton, LM, Nieters, A, North, KE, Novak, AJ, Offit, K, Purdue, MP, Rais, M, Riby, J, Roman, E, Rothman, N, Salles, G, Severi, G, Severson, RK, Skibola, CF, Slager, SL, Smith, A, Smith, MT, Southey, MC, Staines, A, Teras, LR, Thompson, CA, Tilly, H, Tinker, LF, Tjonneland, A, Turner, J, Vajdic, CM, Vermeulen, RCH, Vijai, J, Vineis, P, Virtamo, J, Wang, Z, Weinstein, S, Witzig, TE, Zelenetz, A, Zeleniuch-Jacquotte, A, Zhang, Y, Zheng, T, Zucca, M, Clarke, AE, Bernatsky, S, Garcia, HAV, Spinelli, JJ, Gaffney, P, Smedby, KE, Ramsey-Goldman, R, Wang, SS, Adami, H-O, Albanes, D, Angelucci, E, Ansell, SM, Asmann, YW, Becker, N, Benavente, Y, Berndt, SI, Bertrand, KA, Birmann, BM, Boeing, H, Boffetta, P, Bracci, PM, Brennan, P, Brooks-Wilson, AR, Cerhan, JR, Chanock, SJ, Clavel, J, Conde, L, Cotenbader, KH, Cox, DG, Cozen, W, Crouch, S, De Roos, AJ, de Sanjose, S, Di Lollo, S, Diver, WR, Dogan, A, Foretova, L, Ghesquieres, H, Giles, GG, Glimelius, B, Habermann, TM, Haioun, C, Hartge, P, Hjalgrim, H, Holford, TR, Holly, EA, Jackson, RD, Kaaks, R, Kane, E, Kelly, RS, Klein, RJ, Kraft, P, Kricker, A, Lan, Q, Lawrence, C, Liebow, M, Lightfoot, T, Link, BK, Maynadie, M, Mckay, J, Melbye, M, Molina, TJ, Monnereau, A, Morton, LM, Nieters, A, North, KE, Novak, AJ, Offit, K, Purdue, MP, Rais, M, Riby, J, Roman, E, Rothman, N, Salles, G, Severi, G, Severson, RK, Skibola, CF, Slager, SL, Smith, A, Smith, MT, Southey, MC, Staines, A, Teras, LR, Thompson, CA, Tilly, H, Tinker, LF, Tjonneland, A, Turner, J, Vajdic, CM, Vermeulen, RCH, Vijai, J, Vineis, P, Virtamo, J, Wang, Z, Weinstein, S, Witzig, TE, Zelenetz, A, Zeleniuch-Jacquotte, A, Zhang, Y, Zheng, T, Zucca, M, and Clarke, AE
Abstract: OBJECTIVE: Determinants of the increased risk of diffuse large B-cell lymphoma (DLBCL) in SLE are unclear. Using data from a recent lymphoma genome-wide association study (GWAS), we assessed whether certain lupus-related single nucleotide polymorphisms (SNPs) were also associated with DLBCL. METHODS: GWAS data on European Caucasians from the International Lymphoma Epidemiology Consortium (InterLymph) provided a total of 3857 DLBCL cases and 7666 general-population controls. Data were pooled in a random-effects meta-analysis. RESULTS: Among the 28 SLE-related SNPs investigated, the two most convincingly associated with risk of DLBCL included the CD40 SLE risk allele rs4810485 on chromosome 20q13 (OR per risk allele=1.09, 95% CI 1.02 to 1.16, p=0.0134), and the HLA SLE risk allele rs1270942 on chromosome 6p21.33 (OR per risk allele=1.17, 95% CI 1.01 to 1.36, p=0.0362). Of additional possible interest were rs2205960 and rs12537284. The rs2205960 SNP, related to a cytokine of the tumour necrosis factor superfamily TNFSF4, was associated with an OR per risk allele of 1.07, 95% CI 1.00 to 1.16, p=0.0549. The OR for the rs12537284 (chromosome 7q32, IRF5 gene) risk allele was 1.08, 95% CI 0.99 to 1.18, p=0.0765. CONCLUSIONS: These data suggest several plausible genetic links between DLBCL and SLE.
Published: 2017

32. Compositional analysis of dietary patterns.

Author: Solans, M, Coenders, G, Marcos-Gragera, R, Castelló, A, Gràcia-Lavedan, E, Benavente, Y, Moreno, V, Pérez-Gómez, B, Amiano, P, Fernández-Villa, T, Guevara, M, Gómez-Acebo, I, Fernández-Tardón, G, Vanaclocha-Espi, M, Chirlaque, MD, Capelo, R, Barrios, R, Aragonés, N, Molinuevo, A, and Vitelli-Storelli, F
Subjects: MULTIPLE correspondence analysis (Statistics), DATA analysis
Abstract: Instead of looking at individual nutrients or foods, dietary pattern analysis has emerged as a promising approach to examine the relationship between diet and health outcomes. Despite dietary patterns being compositional (i.e. usually a higher intake of some foods implies that less of other foods are being consumed), compositional data analysis has not yet been applied in this setting. We describe three compositional data analysis approaches (compositional principal component analysis, balances and principal balances) that enable the extraction of dietary patterns by using control subjects from the Spanish multicase-control (MCC-Spain) study. In particular, principal balances overcome the limitations of purely data-driven or investigator-driven methods and present dietary patterns as trade-offs between eating more of some foods and less of others. [ABSTRACT FROM AUTHOR]
Published: 2019
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33. Meta-analysis of genome-wide association studies discovers multiple loci for chronic lymphocytic leukemia

Author: Berndt, SI, Camp, NJ, Skibola, CF, Vijai, J, Wang, Z, Gu, J, Nieters, A, Kelly, RS, Smedby, KE, Monnereau, A, Cozen, W, Cox, A, Wang, SS, Lan, Q, Teras, LR, Machado, M, Yeager, M, Brooks-Wilson, AR, Hartge, P, Purdue, MP, Birmann, BM, Vajdic, CM, Cocco, P, Zhang, Y, Giles, GG, Zeleniuch-Jacquotte, A, Lawrence, C, Montalvan, R, Burdett, L, Hutchinson, A, Ye, Y, Call, TG, Shanafelt, TD, Novak, AJ, Kay, NE, Liebow, M, Cunningham, JM, Allmer, C, Hjalgrim, H, Adami, H-O, Melbye, M, Glimelius, B, Chang, ET, Glenn, M, Curtin, K, Cannon-Albright, LA, Diver, WR, Link, BK, Weiner, GJ, Conde, L, Bracci, PM, Riby, J, Arnett, DK, Zhi, D, Leach, JM, Holly, EA, Jackson, RD, Tinker, LF, Benavente, Y, Sala, N, Casabonne, D, Becker, N, Boffetta, P, Brennan, P, Foretova, L, Maynadie, M, McKay, J, Staines, A, Chaffee, KG, Achenbach, SJ, Vachon, CM, Goldin, LR, Strom, SS, Leis, JF, Weinberg, JB, Caporaso, NE, Norman, AD, De Roos, AJ, Morton, LM, Severson, RK, Riboli, E, Vineis, P, Kaaks, R, Masala, G, Weiderpass, E, Chirlaque, M-D, Vermeulen, RCH, Travis, RC, Southey, MC, Milne, RL, Albanese, D, Virtamo, J, Weinstein, S, Clavel, J, Zheng, T, Holford, TR, Villano, DJ, Maria, A, Spinelli, JJ, Gascoyne, RD, Connors, JM, Bertrand, KA, Giovannucci, E, Kraft, P, Kricker, A, Turner, J, Ennas, MG, Ferri, GM, Miligi, L, Liang, L, Ma, B, Huang, J, Crouch, S, Park, J-H, Chatterjee, N, North, KE, Snowden, JA, Wright, J, Fraumeni, JF, Offit, K, Wu, X, de Sanjose, S, Cerhan, JR, Chanock, SJ, Rothman, N, Slager, SL, Berndt, SI, Camp, NJ, Skibola, CF, Vijai, J, Wang, Z, Gu, J, Nieters, A, Kelly, RS, Smedby, KE, Monnereau, A, Cozen, W, Cox, A, Wang, SS, Lan, Q, Teras, LR, Machado, M, Yeager, M, Brooks-Wilson, AR, Hartge, P, Purdue, MP, Birmann, BM, Vajdic, CM, Cocco, P, Zhang, Y, Giles, GG, Zeleniuch-Jacquotte, A, Lawrence, C, Montalvan, R, Burdett, L, Hutchinson, A, Ye, Y, Call, TG, Shanafelt, TD, Novak, AJ, Kay, NE, Liebow, M, Cunningham, JM, Allmer, C, Hjalgrim, H, Adami, H-O, Melbye, M, Glimelius, B, Chang, ET, Glenn, M, Curtin, K, Cannon-Albright, LA, Diver, WR, Link, BK, Weiner, GJ, Conde, L, Bracci, PM, Riby, J, Arnett, DK, Zhi, D, Leach, JM, Holly, EA, Jackson, RD, Tinker, LF, Benavente, Y, Sala, N, Casabonne, D, Becker, N, Boffetta, P, Brennan, P, Foretova, L, Maynadie, M, McKay, J, Staines, A, Chaffee, KG, Achenbach, SJ, Vachon, CM, Goldin, LR, Strom, SS, Leis, JF, Weinberg, JB, Caporaso, NE, Norman, AD, De Roos, AJ, Morton, LM, Severson, RK, Riboli, E, Vineis, P, Kaaks, R, Masala, G, Weiderpass, E, Chirlaque, M-D, Vermeulen, RCH, Travis, RC, Southey, MC, Milne, RL, Albanese, D, Virtamo, J, Weinstein, S, Clavel, J, Zheng, T, Holford, TR, Villano, DJ, Maria, A, Spinelli, JJ, Gascoyne, RD, Connors, JM, Bertrand, KA, Giovannucci, E, Kraft, P, Kricker, A, Turner, J, Ennas, MG, Ferri, GM, Miligi, L, Liang, L, Ma, B, Huang, J, Crouch, S, Park, J-H, Chatterjee, N, North, KE, Snowden, JA, Wright, J, Fraumeni, JF, Offit, K, Wu, X, de Sanjose, S, Cerhan, JR, Chanock, SJ, Rothman, N, and Slager, SL
Abstract: Chronic lymphocytic leukemia (CLL) is a common lymphoid malignancy with strong heritability. To further understand the genetic susceptibility for CLL and identify common loci associated with risk, we conducted a meta-analysis of four genome-wide association studies (GWAS) composed of 3,100 cases and 7,667 controls with follow-up replication in 1,958 cases and 5,530 controls. Here we report three new loci at 3p24.1 (rs9880772, EOMES, P=2.55 × 10(-11)), 6p25.2 (rs73718779, SERPINB6, P=1.97 × 10(-8)) and 3q28 (rs9815073, LPP, P=3.62 × 10(-8)), as well as a new independent SNP at the known 2q13 locus (rs9308731, BCL2L11, P=1.00 × 10(-11)) in the combined analysis. We find suggestive evidence (P<5 × 10(-7)) for two additional new loci at 4q24 (rs10028805, BANK1, P=7.19 × 10(-8)) and 3p22.2 (rs1274963, CSRNP1, P=2.12 × 10(-7)). Pathway analyses of new and known CLL loci consistently show a strong role for apoptosis, providing further evidence for the importance of this biological pathway in CLL susceptibility.
Published: 2016

34. A meta-analysis of Hodgkin lymphoma reveals 19p13.3 TCF3 as a novel susceptibility locus

Author: Cozen, W., Timofeeva, M. N., Diepstra, A., Hazelett, D., Delahaye-Sourdeix, M., Edlund, C. K., Franke, L., Rostgaard, K., Van Den Berg, D. J., Cortessis, V. K., Smedby, K. E., Glaser, S. L., Westra, H. J., Robison, L. L., Mack, T. M., Ghesquieres, H., Hwang, A. E., Nieters, A., De Sanjose, S., Lightfoot, T., Becker, N., Maynadie, M., Foretova, L., Roman, E., Benavente, Y., Rand, K. A., Nathwani, B. N., Glimelius, B., Staines, A., Boffetta, P., Link, B. K., Kiemeney, L., Ansell, S. M., Bhatia, S., Strong, L. C., Galan, P., Vatten, L., Habermann, T. M., Duell, E. J., Lake, A., Veenstra, R. N., Visser, L., Liu, Y., Urayama, K. Y., Montgomery, D., Gaborieau, V., Weiss, L. M., Byrnes, G., Lathrop, M., Cocco, P., Best, T., Skol, A. D., Adami, H. O., Melbye, M., Cerhan, J. R., Gallagher, A., Taylor, G. M., Slager, S. L., Brennan, P., Coetzee, G. A., Conti, D. V., Onel, K., Jarrett, R. F., Hjalgrim, H., Van Den Berg, A., and McKay, J. D.
Abstract: Recent genome-wide association studies (GWAS) of Hodgkin lymphoma (HL) have identified associations with genetic variation at both HLA and non-HLA loci; however, much of heritable HL susceptibility remains unexplained. Here we perform a meta-analysis of three HL GWAS totaling 1,816 cases and 7,877 controls followed by replication in an independent set of 1,281 cases and 3,218 controls to find novel risk loci. We identify a novel variant at 19p13.3 associated with HL (rs1860661; odds ratio (OR)=0.81, 95% confidence interval (95% CI)=0.76-0.86, P combined =3.5 × 10 10), located in intron 2 of TCF3 (also known as E2A), a regulator of B-and T-cell lineage commitment known to be involved in HL pathogenesis. This meta-analysis also notes associations between previously published loci at 2p16, 5q31, 6p31, 8q24 and 10p14 and HL subtypes. We conclude that our data suggest a link between the 19p13.3 locus, including TCF3, and HL risk.
Published: 2014

35. A Novel Risk Locus at 6p21.3 for Epstein-Barr Virus-Positive Hodgkin Lymphoma

Author: Delahaye-Sourdeix, M., Urayama, K.Y., Gaborieau, V., Veenstra, R., Foll, M., Chabrier, A., Benavente, Y., Nieters, A., Becker, N., Foretova, L., Maynadie, M., Staines, A., Smedby, K.E., Glimelius, I., Lightfoot, T., Cocco, P., Galan, P., Vatten, L.J., Duell, E.J., Kiemeney, L.A., Roman, E., Sanjose, S. de, Lathrop, M., Melbye, M., Brennan, P., Diepstra, A., Berg, A. van den, Hjalgrim, H., Jarrett, R.F., McKay, J.D., Delahaye-Sourdeix, M., Urayama, K.Y., Gaborieau, V., Veenstra, R., Foll, M., Chabrier, A., Benavente, Y., Nieters, A., Becker, N., Foretova, L., Maynadie, M., Staines, A., Smedby, K.E., Glimelius, I., Lightfoot, T., Cocco, P., Galan, P., Vatten, L.J., Duell, E.J., Kiemeney, L.A., Roman, E., Sanjose, S. de, Lathrop, M., Melbye, M., Brennan, P., Diepstra, A., Berg, A. van den, Hjalgrim, H., Jarrett, R.F., and McKay, J.D.
Abstract: Item does not contain fulltext, BACKGROUND: A proportion of the genetic variants involved in susceptibility to Hodgkin lymphoma differ by the tumor's Epstein-Barr virus (EBV) status, particularly within the MHC region. METHODS: We have conducted an SNP imputation study of the MHC region, considering tumor EBV status in 1,200 classical Hodgkin lymphoma (cHL) cases and 5,726 control subjects of European origin. Notable findings were genotyped in an independent study population of 468 cHL cases and 551 controls. RESULTS: We identified and subsequently replicated a novel association between a common genetic variant rs6457715 and cHL. Although strongly associated with EBV-positive cHL [OR, 2.33; 95% confidence interval (CI), 1.83-2.97; P = 7 x 10(-12)], there was little evidence for association between rs6457715 and the EBV-negative subgroup of cHL (OR, 1.06; 95% CI, 0.92-1.21), indicating that this association was specific to the EBV-positive subgroup (Phet < P = 10(-8)). Furthermore, the association was limited to EBV-positive cHL subgroups within mixed cell (MCHL) and nodular sclerosis subtypes (NSHL), suggesting that the association is independent of histologic subtype of cHL. CONCLUSIONS: rs6457715, located near the HLA-DPB1 gene, is associated with EBV-positive cHL and suggests this region as a novel susceptibility locus for cHL. IMPACT: This expands the number of genetic variants that are associated with cHL and provides additional evidence for a critical and specific role of EBV in the etiology of this disease. Cancer Epidemiol Biomarkers Prev; 24(12); 1838-43. (c)2015 AACR.
Published: 2015

36. A genome-wide association study of marginal zone lymphoma shows association to the HLA region

Author: Vijai, J, Wang, Z, Berndt, SI, Skibola, CF, Slager, SL, de Sanjose, S, Melbye, M, Glimelius, B, Bracci, PM, Conde, L, Birmann, BM, Wang, SS, Brooks-Wilson, AR, Lan, Q, de Bakker, PIW, Vermeulen, RCH, Portlock, C, Ansell, SM, Link, BK, Riby, J, North, KE, Gu, J, Hjalgrim, H, Cozen, W, Becker, N, Teras, LR, Spinelli, JJ, Turner, J, Zhang, Y, Purdue, MP, Giles, GG, Kelly, RS, Zeleniuch-Jacquotte, A, Ennas, MG, Monnereau, A, Bertrand, KA, Albanes, D, Lightfoot, T, Yeager, M, Chung, CC, Burdett, L, Hutchinson, A, Lawrence, C, Montalvan, R, Liang, L, Huang, J, Ma, B, Villano, DJ, Maria, A, Corines, M, Thomas, T, Novak, AJ, Dogan, A, Liebow, M, Thompson, CA, Witzig, TE, Habermann, TM, Weiner, GJ, Smith, MT, Holly, EA, Jackson, RD, Tinker, LF, Ye, Y, Adami, H-O, Smedby, KE, De Roos, AJ, Hartge, P, Morton, LM, Severson, RK, Benavente, Y, Boffetta, P, Brennan, P, Foretova, L, Maynadie, M, Mckay, J, Staines, A, Diver, WR, Vajdic, CM, Armstrong, BK, Kricker, A, Zheng, T, Holford, TR, Severi, G, Vineis, P, Ferri, GM, Ricco, R, Miligi, L, Clavel, J, Giovannucci, E, Kraft, P, Virtamo, J, Smith, A, Kane, E, Roman, E, Chiu, BCH, Fraumeni, JF, Wu, X, Cerhan, JR, Offit, K, Chanock, SJ, Rothman, N, Nieters, A, Vijai, J, Wang, Z, Berndt, SI, Skibola, CF, Slager, SL, de Sanjose, S, Melbye, M, Glimelius, B, Bracci, PM, Conde, L, Birmann, BM, Wang, SS, Brooks-Wilson, AR, Lan, Q, de Bakker, PIW, Vermeulen, RCH, Portlock, C, Ansell, SM, Link, BK, Riby, J, North, KE, Gu, J, Hjalgrim, H, Cozen, W, Becker, N, Teras, LR, Spinelli, JJ, Turner, J, Zhang, Y, Purdue, MP, Giles, GG, Kelly, RS, Zeleniuch-Jacquotte, A, Ennas, MG, Monnereau, A, Bertrand, KA, Albanes, D, Lightfoot, T, Yeager, M, Chung, CC, Burdett, L, Hutchinson, A, Lawrence, C, Montalvan, R, Liang, L, Huang, J, Ma, B, Villano, DJ, Maria, A, Corines, M, Thomas, T, Novak, AJ, Dogan, A, Liebow, M, Thompson, CA, Witzig, TE, Habermann, TM, Weiner, GJ, Smith, MT, Holly, EA, Jackson, RD, Tinker, LF, Ye, Y, Adami, H-O, Smedby, KE, De Roos, AJ, Hartge, P, Morton, LM, Severson, RK, Benavente, Y, Boffetta, P, Brennan, P, Foretova, L, Maynadie, M, Mckay, J, Staines, A, Diver, WR, Vajdic, CM, Armstrong, BK, Kricker, A, Zheng, T, Holford, TR, Severi, G, Vineis, P, Ferri, GM, Ricco, R, Miligi, L, Clavel, J, Giovannucci, E, Kraft, P, Virtamo, J, Smith, A, Kane, E, Roman, E, Chiu, BCH, Fraumeni, JF, Wu, X, Cerhan, JR, Offit, K, Chanock, SJ, Rothman, N, and Nieters, A
Abstract: Marginal zone lymphoma (MZL) is the third most common subtype of B-cell non-Hodgkin lymphoma. Here we perform a two-stage GWAS of 1,281 MZL cases and 7,127 controls of European ancestry and identify two independent loci near BTNL2 (rs9461741, P=3.95 × 10(-15)) and HLA-B (rs2922994, P=2.43 × 10(-9)) in the HLA region significantly associated with MZL risk. This is the first evidence that genetic variation in the major histocompatibility complex influences MZL susceptibility.
Published: 2015

37. Genome-wide association study identifies multiple risk loci for chronic lymphocytic leukemia

Author: Berndt, S.I., Skibola, C.F., Joseph, V., Camp, N.J., Nieters, A., Wang, Z., Cozen, W., Monnereau, A., Wang, S.S., Kelly, R.S., Lan, Q., Teras, L.R., Chatterjee, N., Chung, C.C., Yeager, M., Brooks-Wilson, A.R., Hartge, P., Purdue, M.P., Birmann, B.M., Armstrong, B.K., Cocco, P., Zhang, Y., Severi, G., Zeleniuch-Jacquotte, A., Lawrence, C., Burdette, L., Yuenger, J., Hutchinson, A., Jacobs, K.B., Call, T.G., Shanafelt, T.D., Novak, A.J., Kay, N.E., Liebow, M., Wang, A.H., Smedby, K.E., Adami, H.-O., Melbye, M., Glimelius, B., Chang, E.T., Glenn, M., Curtin, K., Cannon-Albright, L.A., Jones, B., Diver, W.R., Link, B.K., Weiner, G.J., Conde, L., Bracci, P.M., Riby, J., Holly, E.A., Smith, M.T., Jackson, R.D., Tinker, L.F., Benavente, Y., Becker, N., Boffetta, P., Brennan, P., Foretova, L., Maynadie, M., McKay, J., Staines, A., Rabe, K.G., Achenbach, S.J., Vachon, C.M., Goldin, L.R., Strom, S.S., Lanasa, M.C., Spector, L.G., Leis, J.F., Cunningham, J.M., Weinberg, J.B., Morrison, V.A., Caporaso, N.E., Norman, A.D., Linet, M.S., De Roos, A.J., Morton, L.M., Severson, R.K., Riboli, E., Vineis, P., Kaaks, R., Trichopoulos, D., Masala, G., Weiderpass, E., Chirlaque, M.-D., Vermeulen, R.C.H., Travis, R.C., Giles, G.G., Albanes, D., Virtamo, J., Weinstein, S., Clavel, J., Zheng, T., Holford, T.R., Offit, K., Zelenetz, A., Klein, R.J., Spinelli, J.J., Bertrand, K.A., Laden, F., Giovannucci, E., Kraft, P., Kricker, A., Turner, J., Vajdic, C.M., Ennas, M.G., Ferri, G.M., Miligi, L., Liang, L., Sampson, J., Crouch, S., Park, J.-H., North, K.E., Cox, A., Snowden, J.A., Wright, J., Carracedo, A., Lopez-Otin, C., Bea, S., Salaverria, I., Martin-Garcia, D., Campo, E., Jr, F.J.F., de Sanjose, S., Hjalgrim, H., Cerhan, J.R., Chanock, S.J., Rothman, N., and Slager, S.L.
Abstract: Genome-wide association studies (GWAS) have previously identified 13 loci associated with risk of chronic lymphocytic leukemia or small lymphocytic lymphoma (CLL). To identify additional CLL susceptibility loci, we conducted the largest meta-analysis for CLL thus far, including four GWAS with a total of 3,100 individuals with CLL (cases) and 7,667 controls. In the meta-analysis, we identified ten independent associated SNPs in nine new loci at 10q23.31 (ACTA2 or FAS (ACTA2/FAS), P = 1.22 × 10−14), 18q21.33 (BCL2, P = 7.76 × 10−11), 11p15.5 (C11orf21, P = 2.15 × 10−10), 4q25 (LEF1, P = 4.24 × 10−10), 2q33.1 (CASP10 or CASP8 (CASP10/CASP8), P = 2.50 × 10−9), 9p21.3 (CDKN2B-AS1, P = 1.27 × 10−8), 18q21.32 (PMAIP1, P = 2.51 × 10−8), 15q15.1 (BMF, P = 2.71 × 10−10) and 2p22.2 (QPCT, P = 1.68 × 10−8), as well as an independent signal at an established locus (2q13, ACOXL, P = 2.08 × 10−18). We also found evidence for two additional promising loci below genome-wide significance at 8q22.3 (ODF1, P = 5.40 × 10−8) and 5p15.33 (TERT, P = 1.92 × 10−7). Although further studies are required, the proximity of several of these loci to genes involved in apoptosis suggests a plausible underlying biological mechanism.
Published: 2013

38. Occupational exposure to endocrine disruptors and lymphoma risk in a multi-centric European study

Author: Costas, L, primary, Infante-Rivard, C, additional, Zock, J-P, additional, Van Tongeren, M, additional, Boffetta, P, additional, Cusson, A, additional, Robles, C, additional, Casabonne, D, additional, Benavente, Y, additional, Becker, N, additional, Brennan, P, additional, Foretova, L, additional, Maynadié, M, additional, Staines, A, additional, Nieters, A, additional, Cocco, P, additional, and de Sanjosé, S, additional
Published: 2015
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39. Genome-wide association study identifies multiple susceptibility loci for diffuse large B cell lymphoma

Author: Cerhan, JR, Berndt, SI, Vijai, J, Ghesquieres, H, McKay, J, Wang, SS, Wang, Z, Yeager, M, Conde, L, de Bakker, PIW, Nieters, A, Cox, D, Burdett, L, Monnereau, A, Flowers, CR, De Roos, AJ, Brooks-Wilson, AR, Lan, Q, Severi, G, Melbye, M, Gu, J, Jackson, RD, Kane, E, Teras, LR, Purdue, MP, Vajdic, CM, Spinelli, JJ, Giles, GG, Albanes, D, Kelly, RS, Zucca, M, Bertrand, KA, Zeleniuch-Jacquotte, A, Lawrence, C, Hutchinson, A, Zhi, D, Habermann, TM, Link, BK, Novak, AJ, Dogan, A, Asmann, YW, Liebow, M, Thompson, CA, Ansell, SM, Witzig, TE, Weiner, GJ, Veron, AS, Zelenika, D, Tilly, H, Haioun, C, Molina, TJ, Hjalgrim, H, Glimelius, B, Adami, H-O, Bracci, PM, Riby, J, Smith, MT, Holly, EA, Cozen, W, Hartge, P, Morton, LM, Severson, RK, Tinker, LF, North, KE, Becker, N, Benavente, Y, Boffetta, P, Brennan, P, Foretova, L, Maynadie, M, Staines, A, Lightfoot, T, Crouch, S, Smith, A, Roman, E, Diver, WR, Offit, K, Zelenetz, A, Klein, RJ, Villano, DJ, Zheng, T, Zhang, Y, Holford, TR, Kricker, A, Turner, J, Southey, MC, Clavel, J, Virtamo, J, Weinstein, S, Riboli, E, Vineis, P, Kaaks, R, Trichopoulos, D, Vermeulen, RCH, Boeing, H, Tjonneland, A, Angelucci, E, Di Lollo, S, Rais, M, Birmann, BM, Laden, F, Giovannucci, E, Kraft, P, Huang, J, Ma, B, Ye, Y, Chiu, BCH, Sampson, J, Liang, L, Park, J-H, Chung, CC, Weisenburger, DD, Chatterjee, N, Fraumeni, JF, Slager, SL, Wu, X, de Sanjose, S, Smedby, KE, Salles, G, Skibola, CF, Rothman, N, Chanock, SJ, Cerhan, JR, Berndt, SI, Vijai, J, Ghesquieres, H, McKay, J, Wang, SS, Wang, Z, Yeager, M, Conde, L, de Bakker, PIW, Nieters, A, Cox, D, Burdett, L, Monnereau, A, Flowers, CR, De Roos, AJ, Brooks-Wilson, AR, Lan, Q, Severi, G, Melbye, M, Gu, J, Jackson, RD, Kane, E, Teras, LR, Purdue, MP, Vajdic, CM, Spinelli, JJ, Giles, GG, Albanes, D, Kelly, RS, Zucca, M, Bertrand, KA, Zeleniuch-Jacquotte, A, Lawrence, C, Hutchinson, A, Zhi, D, Habermann, TM, Link, BK, Novak, AJ, Dogan, A, Asmann, YW, Liebow, M, Thompson, CA, Ansell, SM, Witzig, TE, Weiner, GJ, Veron, AS, Zelenika, D, Tilly, H, Haioun, C, Molina, TJ, Hjalgrim, H, Glimelius, B, Adami, H-O, Bracci, PM, Riby, J, Smith, MT, Holly, EA, Cozen, W, Hartge, P, Morton, LM, Severson, RK, Tinker, LF, North, KE, Becker, N, Benavente, Y, Boffetta, P, Brennan, P, Foretova, L, Maynadie, M, Staines, A, Lightfoot, T, Crouch, S, Smith, A, Roman, E, Diver, WR, Offit, K, Zelenetz, A, Klein, RJ, Villano, DJ, Zheng, T, Zhang, Y, Holford, TR, Kricker, A, Turner, J, Southey, MC, Clavel, J, Virtamo, J, Weinstein, S, Riboli, E, Vineis, P, Kaaks, R, Trichopoulos, D, Vermeulen, RCH, Boeing, H, Tjonneland, A, Angelucci, E, Di Lollo, S, Rais, M, Birmann, BM, Laden, F, Giovannucci, E, Kraft, P, Huang, J, Ma, B, Ye, Y, Chiu, BCH, Sampson, J, Liang, L, Park, J-H, Chung, CC, Weisenburger, DD, Chatterjee, N, Fraumeni, JF, Slager, SL, Wu, X, de Sanjose, S, Smedby, KE, Salles, G, Skibola, CF, Rothman, N, and Chanock, SJ
Abstract: Diffuse large B cell lymphoma (DLBCL) is the most common lymphoma subtype and is clinically aggressive. To identify genetic susceptibility loci for DLBCL, we conducted a meta-analysis of 3 new genome-wide association studies (GWAS) and 1 previous scan, totaling 3,857 cases and 7,666 controls of European ancestry, with additional genotyping of 9 promising SNPs in 1,359 cases and 4,557 controls. In our multi-stage analysis, five independent SNPs in four loci achieved genome-wide significance marked by rs116446171 at 6p25.3 (EXOC2; P = 2.33 × 10(-21)), rs2523607 at 6p21.33 (HLA-B; P = 2.40 × 10(-10)), rs79480871 at 2p23.3 (NCOA1; P = 4.23 × 10(-8)) and two independent SNPs, rs13255292 and rs4733601, at 8q24.21 (PVT1; P = 9.98 × 10(-13) and 3.63 × 10(-11), respectively). These data provide substantial new evidence for genetic susceptibility to this B cell malignancy and point to pathways involved in immune recognition and immune function in the pathogenesis of DLBCL.
Published: 2014

40. Medical History, Lifestyle, Family History, and Occupational Risk Factors for Follicular Lymphoma: The InterLymph Non-Hodgkin Lymphoma Subtypes Project

Author: Linet, M. S., primary, Vajdic, C. M., additional, Morton, L. M., additional, de Roos, A. J., additional, Skibola, C. F., additional, Boffetta, P., additional, Cerhan, J. R., additional, Flowers, C. R., additional, de Sanjose, S., additional, Monnereau, A., additional, Cocco, P., additional, Kelly, J. L., additional, Smith, A. G., additional, Weisenburger, D. D., additional, Clarke, C. A., additional, Blair, A., additional, Bernstein, L., additional, Zheng, T., additional, Miligi, L., additional, Clavel, J., additional, Benavente, Y., additional, and Chiu, B. C. H., additional
Published: 2014
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41. Medical History, Lifestyle, Family History, and Occupational Risk Factors for Chronic Lymphocytic Leukemia/Small Lymphocytic Lymphoma: The InterLymph Non-Hodgkin Lymphoma Subtypes Project

Author: Slager, S. L., primary, Benavente, Y., additional, Blair, A., additional, Vermeulen, R., additional, Cerhan, J. R., additional, Costantini, A. S., additional, Monnereau, A., additional, Nieters, A., additional, Clavel, J., additional, Call, T. G., additional, Maynadie, M., additional, Lan, Q., additional, Clarke, C. A., additional, Lightfoot, T., additional, Norman, A. D., additional, Sampson, J. N., additional, Casabonne, D., additional, Cocco, P., additional, and de Sanjose, S., additional
Published: 2014
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42. Rationale and Design of the International Lymphoma Epidemiology Consortium (InterLymph) Non-Hodgkin Lymphoma Subtypes Project

Author: Morton, L. M., primary, Sampson, J. N., additional, Cerhan, J. R., additional, Turner, J. J., additional, Vajdic, C. M., additional, Wang, S. S., additional, Smedby, K. E., additional, de Sanjose, S., additional, Monnereau, A., additional, Benavente, Y., additional, Bracci, P. M., additional, Chiu, B. C. H., additional, Skibola, C. F., additional, Zhang, Y., additional, Mbulaiteye, S. M., additional, Spriggs, M., additional, Robinson, D., additional, Norman, A. D., additional, Kane, E. V., additional, Spinelli, J. J., additional, Kelly, J. L., additional, Vecchia, C. L., additional, Dal Maso, L., additional, Maynadie, M., additional, Kadin, M. E., additional, Cocco, P., additional, Costantini, A. S., additional, Clarke, C. A., additional, Roman, E., additional, Miligi, L., additional, Colt, J. S., additional, Berndt, S. I., additional, Mannetje, A., additional, de Roos, A. J., additional, Kricker, A., additional, Nieters, A., additional, Franceschi, S., additional, Melbye, M., additional, Boffetta, P., additional, Clavel, J., additional, Linet, M. S., additional, Weisenburger, D. D., additional, and Slager, S. L., additional
Published: 2014
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43. Medical History, Lifestyle, Family History, and Occupational Risk Factors for Marginal Zone Lymphoma: The InterLymph Non-Hodgkin Lymphoma Subtypes Project

Author: Bracci, P. M., primary, Benavente, Y., additional, Turner, J. J., additional, Paltiel, O., additional, Slager, S. L., additional, Vajdic, C. M., additional, Norman, A. D., additional, Cerhan, J. R., additional, Chiu, B. C. H., additional, Becker, N., additional, Cocco, P., additional, Dogan, A., additional, Nieters, A., additional, Holly, E. A., additional, Kane, E. V., additional, Smedby, K. E., additional, Maynadie, M., additional, Spinelli, J. J., additional, Roman, E., additional, Glimelius, B., additional, Wang, S. S., additional, Sampson, J. N., additional, Morton, L. M., additional, and de Sanjose, S., additional
Published: 2014
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44. Etiologic Heterogeneity Among Non-Hodgkin Lymphoma Subtypes: The InterLymph Non-Hodgkin Lymphoma Subtypes Project

Author: Morton, L. M., primary, Slager, S. L., additional, Cerhan, J. R., additional, Wang, S. S., additional, Vajdic, C. M., additional, Skibola, C. F., additional, Bracci, P. M., additional, de Sanjose, S., additional, Smedby, K. E., additional, Chiu, B. C. H., additional, Zhang, Y., additional, Mbulaiteye, S. M., additional, Monnereau, A., additional, Turner, J. J., additional, Clavel, J., additional, Adami, H.-O., additional, Chang, E. T., additional, Glimelius, B., additional, Hjalgrim, H., additional, Melbye, M., additional, Crosignani, P., additional, di Lollo, S., additional, Miligi, L., additional, Nanni, O., additional, Ramazzotti, V., additional, Rodella, S., additional, Costantini, A. S., additional, Stagnaro, E., additional, Tumino, R., additional, Vindigni, C., additional, Vineis, P., additional, Becker, N., additional, Benavente, Y., additional, Boffetta, P., additional, Brennan, P., additional, Cocco, P., additional, Foretova, L., additional, Maynadie, M., additional, Nieters, A., additional, Staines, A., additional, Colt, J. S., additional, Cozen, W., additional, Davis, S., additional, de Roos, A. J., additional, Hartge, P., additional, Rothman, N., additional, Severson, R. K., additional, Holly, E. A., additional, Call, T. G., additional, Feldman, A. L., additional, Habermann, T. M., additional, Liebow, M., additional, Blair, A., additional, Cantor, K. P., additional, Kane, E. V., additional, Lightfoot, T., additional, Roman, E., additional, Smith, A., additional, Brooks-Wilson, A., additional, Connors, J. M., additional, Gascoyne, R. D., additional, Spinelli, J. J., additional, Armstrong, B. K., additional, Kricker, A., additional, Holford, T. R., additional, Lan, Q., additional, Zheng, T., additional, Orsi, L., additional, Dal Maso, L., additional, Franceschi, S., additional, La Vecchia, C., additional, Negri, E., additional, Serraino, D., additional, Bernstein, L., additional, Levine, A., additional, Friedberg, J. W., additional, Kelly, J. L., additional, Berndt, S. I., additional, Birmann, B. M., additional, Clarke, C. A., additional, Flowers, C. R., additional, Foran, J. M., additional, Kadin, M. E., additional, Paltiel, O., additional, Weisenburger, D. D., additional, Linet, M. S., additional, and Sampson, J. N., additional
Published: 2014
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45. Genome-wide association study identifies multiple risk loci for chronic lymphocytic leukemia

Author: Berndt, SI, Skibola, CF, Joseph, V, Camp, NJ, Nieters, A, Wang, Z, Cozen, W, Monnereau, A, Wang, SS, Kelly, RS, Lan, Q, Teras, LR, Chatterjee, N, Chung, CC, Yeager, M, Brooks-Wilson, AR, Hartge, P, Purdue, MP, Birmann, BM, Armstrong, BK, Cocco, P, Zhang, Y, Severi, G, Zeleniuch-Jacquotte, A, Lawrence, C, Burdette, L, Yuenger, J, Hutchinson, A, Jacobs, KB, Call, TG, Shanafelt, TD, Novak, AJ, Kay, NE, Liebow, M, Wang, AH, Smedby, KE, Adami, H-O, Melbye, M, Glimelius, B, Chang, ET, Glenn, M, Curtin, K, Cannon-Albright, LA, Jones, B, Diver, WR, Link, BK, Weiner, GJ, Conde, L, Bracci, PM, Riby, J, Holly, EA, Smith, MT, Jackson, RD, Tinker, LF, Benavente, Y, Becker, N, Boffetta, P, Brennan, P, Foretova, L, Maynadie, M, McKay, J, Staines, A, Rabe, KG, Achenbach, SJ, Vachon, CM, Goldin, LR, Strom, SS, Lanasa, MC, Spector, LG, Leis, JF, Cunningham, JM, Weinberg, JB, Morrison, VA, Caporaso, NE, Norman, AD, Linet, MS, De Roos, AJ, Morton, LM, Severson, RK, Riboli, E, Vineis, P, Kaaks, R, Trichopoulos, D, Masala, G, Weiderpass, E, Chirlaque, M-D, Vermeulen, RCH, Travis, RC, Giles, GG, Albanes, D, Virtamo, J, Weinstein, S, Clavel, J, Zheng, T, Holford, TR, Offit, K, Zelenetz, A, Klein, RJ, Spinelli, JJ, Bertrand, KA, Laden, F, Giovannucci, E, Kraft, P, Kricker, A, Turner, J, Vajdic, CM, Ennas, MG, Ferri, GM, Miligi, L, Liang, L, Sampson, J, Crouch, S, Park, J-H, North, KE, Cox, A, Snowden, JA, Wright, J, Carracedo, A, Lopez-Otin, C, Bea, S, Salaverria, I, Martin-Garcia, D, Campo, E, Fraumeni, JF, de Sanjose, S, Hjalgrim, H, Cerhan, JR, Chanock, SJ, Rothman, N, Slager, SL, Berndt, SI, Skibola, CF, Joseph, V, Camp, NJ, Nieters, A, Wang, Z, Cozen, W, Monnereau, A, Wang, SS, Kelly, RS, Lan, Q, Teras, LR, Chatterjee, N, Chung, CC, Yeager, M, Brooks-Wilson, AR, Hartge, P, Purdue, MP, Birmann, BM, Armstrong, BK, Cocco, P, Zhang, Y, Severi, G, Zeleniuch-Jacquotte, A, Lawrence, C, Burdette, L, Yuenger, J, Hutchinson, A, Jacobs, KB, Call, TG, Shanafelt, TD, Novak, AJ, Kay, NE, Liebow, M, Wang, AH, Smedby, KE, Adami, H-O, Melbye, M, Glimelius, B, Chang, ET, Glenn, M, Curtin, K, Cannon-Albright, LA, Jones, B, Diver, WR, Link, BK, Weiner, GJ, Conde, L, Bracci, PM, Riby, J, Holly, EA, Smith, MT, Jackson, RD, Tinker, LF, Benavente, Y, Becker, N, Boffetta, P, Brennan, P, Foretova, L, Maynadie, M, McKay, J, Staines, A, Rabe, KG, Achenbach, SJ, Vachon, CM, Goldin, LR, Strom, SS, Lanasa, MC, Spector, LG, Leis, JF, Cunningham, JM, Weinberg, JB, Morrison, VA, Caporaso, NE, Norman, AD, Linet, MS, De Roos, AJ, Morton, LM, Severson, RK, Riboli, E, Vineis, P, Kaaks, R, Trichopoulos, D, Masala, G, Weiderpass, E, Chirlaque, M-D, Vermeulen, RCH, Travis, RC, Giles, GG, Albanes, D, Virtamo, J, Weinstein, S, Clavel, J, Zheng, T, Holford, TR, Offit, K, Zelenetz, A, Klein, RJ, Spinelli, JJ, Bertrand, KA, Laden, F, Giovannucci, E, Kraft, P, Kricker, A, Turner, J, Vajdic, CM, Ennas, MG, Ferri, GM, Miligi, L, Liang, L, Sampson, J, Crouch, S, Park, J-H, North, KE, Cox, A, Snowden, JA, Wright, J, Carracedo, A, Lopez-Otin, C, Bea, S, Salaverria, I, Martin-Garcia, D, Campo, E, Fraumeni, JF, de Sanjose, S, Hjalgrim, H, Cerhan, JR, Chanock, SJ, Rothman, N, and Slager, SL
Abstract: Genome-wide association studies (GWAS) have previously identified 13 loci associated with risk of chronic lymphocytic leukemia or small lymphocytic lymphoma (CLL). To identify additional CLL susceptibility loci, we conducted the largest meta-analysis for CLL thus far, including four GWAS with a total of 3,100 individuals with CLL (cases) and 7,667 controls. In the meta-analysis, we identified ten independent associated SNPs in nine new loci at 10q23.31 (ACTA2 or FAS (ACTA2/FAS), P=1.22×10(-14)), 18q21.33 (BCL2, P=7.76×10(-11)), 11p15.5 (C11orf21, P=2.15×10(-10)), 4q25 (LEF1, P=4.24×10(-10)), 2q33.1 (CASP10 or CASP8 (CASP10/CASP8), P=2.50×10(-9)), 9p21.3 (CDKN2B-AS1, P=1.27×10(-8)), 18q21.32 (PMAIP1, P=2.51×10(-8)), 15q15.1 (BMF, P=2.71×10(-10)) and 2p22.2 (QPCT, P=1.68×10(-8)), as well as an independent signal at an established locus (2q13, ACOXL, P=2.08×10(-18)). We also found evidence for two additional promising loci below genome-wide significance at 8q22.3 (ODF1, P=5.40×10(-8)) and 5p15.33 (TERT, P=1.92×10(-7)). Although further studies are required, the proximity of several of these loci to genes involved in apoptosis suggests a plausible underlying biological mechanism.
Published: 2013

46. Genome-wide association study of classical Hodgkin lymphoma and Epstein-Barr virus status-defined subgroups.

Author: Urayama, K.Y., Jarrett, R.F., Hjalgrim, H., Diepstra, A., Kamatani, Y., Chabrier, A., Gaborieau, V., Boland, A., Nieters, A., Becker, N., Foretova, L., Benavente, Y., Maynadie, M., Staines, A., Shield, L., Lake, A., Montgomery, D., Taylor, M., Smedby, K.E., Amini, R.M., Adami, H.O., Glimelius, B., Feenstra, B., Nolte, I.M., Visser, L., Imhoff, G.W. van, Lightfoot, T., Cocco, P., Kiemeney, L.A., Vermeulen, S., Holcatova, I., Vatten, L., Macfarlane, G.J., Thomson, P., Conway, D.I., Benhamou, S., Agudo, A., Healy, C.M., Overvad, K., Tjonneland, A., Melin, B., Canzian, F., Khaw, K.T., Travis, R.C., Peeters, P.H.M., Gonzalez, C.A., Quiros, J.R., Sanchez, M.J., Huerta, J.M., Ardanaz, E., Dorronsoro, M., Clavel-Chapelon, F., Bueno-De-Mesquita, H.B., Riboli, E., Roman, E., Boffetta, P., Sanjose, S. de, Zelenika, D., Melbye, M., Berg, A. van den, Lathrop, M., Brennan, P., McKay, J.D., Urayama, K.Y., Jarrett, R.F., Hjalgrim, H., Diepstra, A., Kamatani, Y., Chabrier, A., Gaborieau, V., Boland, A., Nieters, A., Becker, N., Foretova, L., Benavente, Y., Maynadie, M., Staines, A., Shield, L., Lake, A., Montgomery, D., Taylor, M., Smedby, K.E., Amini, R.M., Adami, H.O., Glimelius, B., Feenstra, B., Nolte, I.M., Visser, L., Imhoff, G.W. van, Lightfoot, T., Cocco, P., Kiemeney, L.A., Vermeulen, S., Holcatova, I., Vatten, L., Macfarlane, G.J., Thomson, P., Conway, D.I., Benhamou, S., Agudo, A., Healy, C.M., Overvad, K., Tjonneland, A., Melin, B., Canzian, F., Khaw, K.T., Travis, R.C., Peeters, P.H.M., Gonzalez, C.A., Quiros, J.R., Sanchez, M.J., Huerta, J.M., Ardanaz, E., Dorronsoro, M., Clavel-Chapelon, F., Bueno-De-Mesquita, H.B., Riboli, E., Roman, E., Boffetta, P., Sanjose, S. de, Zelenika, D., Melbye, M., Berg, A. van den, Lathrop, M., Brennan, P., and McKay, J.D.
Abstract: Item does not contain fulltext, BACKGROUND: Accumulating evidence suggests that risk factors for classical Hodgkin lymphoma (cHL) differ by tumor Epstein-Barr virus (EBV) status. This potential etiological heterogeneity is not recognized in current disease classification. METHODS: We conducted a genome-wide association study of 1200 cHL patients and 6417 control subjects, with validation in an independent replication series, to identify common genetic variants associated with total cHL and subtypes defined by tumor EBV status. Multiple logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs) assuming a log-additive genetic model for the variants. All statistical tests were two-sided. RESULTS: Two novel loci associated with total cHL irrespective of EBV status were identified in the major histocompatibility complex region; one resides adjacent to MICB (rs2248462: OR = 0.61, 95% CI = 0.53 to 0.69, P = 1.3 x 10(-13)) and the other at HLA-DRA (rs2395185: OR = 0.56, 95% CI = 0.50 to 0.62, P = 8.3 x 10(-25)) with both results confirmed in an independent replication series. Consistent with previous reports, associations were found between EBV-positive cHL and genetic variants within the class I region (rs2734986, HLA-A: OR = 2.45, 95% CI = 2.00 to 3.00, P = 1.2 x 10(-15); rs6904029, HCG9: OR = 0.46, 95% CI = 0.36 to 0.59, P = 5.5 x 10(-10)) and between EBV-negative cHL and rs6903608 within the class II region (rs6903608, HLA-DRA: OR = 2.08, 95% CI = 1.84 to 2.35, P = 6.1 x 10(-31)). The association between rs6903608 and EBV-negative cHL was confined to the nodular sclerosis histological subtype. Evidence for an association between EBV-negative cHL and rs20541 (5q31, IL13: OR = 1.53, 95% CI = 1.32 to 1.76, P = 5.4 x 10(-9)), a variant previously linked to psoriasis and asthma, was observed; however, the evidence for replication was less clear. Notably, one additional psoriasis-associated variant, rs27524 (5q15, ERAP1), showed evidence of an association with cHL in the
Published: 2012

47. Polymorphisms in DNA repair genes modify lymphoma risk

Author: Butterbach, K, Popanda, O, de Sanjosé, S, Benavente, Y, Becker, N, Foretova, L, Maynadie, M, Cocco, P, Staines, A, Kaaks, R, Hieke, S, Schumacher, M, Boffetta, P, Brennan, P, Nieters, A, Butterbach, K, Popanda, O, de Sanjosé, S, Benavente, Y, Becker, N, Foretova, L, Maynadie, M, Cocco, P, Staines, A, Kaaks, R, Hieke, S, Schumacher, M, Boffetta, P, Brennan, P, and Nieters, A
Published: 2011

48. Association of NOS2 and potential effect of VEGF, IL6, CCL2 and IL1RN polymorphisms and haplotypes on susceptibility to GCA--a simultaneous study of 130 potentially functional SNPs in 14 candidate genes

Author: Enjuanes, A., primary, Benavente, Y., additional, Hernandez-Rodriguez, J., additional, Queralt, C., additional, Yague, J., additional, Jares, P., additional, de Sanjose, S., additional, Campo, E., additional, and Cid, M. C., additional
Published: 2012
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49. 3.10 Risk Factors Associated with Chronic Lymphocytic Leukaemia in a Spanish Case−Control Study (MCC−Spain)

Author: Benavente, Y., primary, Casabonne, D., additional, Robles, C., additional, Costas, L., additional, Aymerich, M., additional, Peiró-Pérez, R., additional, Gomez-Acebo, I., additional, López Guillermo, A., additional, Tardón, A., additional, Salar, A., additional, Pollán, M., additional, Kogevinas, M., additional, Lopez-Otín, C., additional, Campo, E., additional, and denome Pe Sanjosé, S., additional
Published: 2011
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50. Antibodies against lytic and latent Kaposi's sarcoma-associated herpes virus antigens and lymphoma in the European EpiLymph case–control study

Author: Benavente, Y, primary, Mbisa, G, additional, Labo, N, additional, Casabonne, D, additional, Becker, N, additional, Maynadie, M, additional, Foretova, L, additional, Cocco, P L, additional, Nieters, A, additional, Staines, A, additional, Bofetta, P, additional, Brennan, P, additional, Whitby, D, additional, and de Sanjosé, S, additional
Published: 2011
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