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1. Antimicrobial Activities of Chloroform Extract of Whole Plant of Sida acuta Burm. f against Selected Clinical Isolates from Laboratory Samples of a Private Hospital in Benin City, Edo State, Nigeria

Author: Timothy, O., primary, Obazee, O. J., additional, Oghama, O. E., additional, and Odaro, J. O., additional
Published: 2023
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2. Genetic determinants of telomere length and risk of pancreatic cancer: A PANDoRA study

Author: Campa, D, Matarazzi, M, Greenhalf, W, Bijlsma, M, Saum, K-U, Pasquali, C, Van Laarhoven, H, Szentesi, A, Federici, F, Vodicka, P, Funel, N, Pezzilli, R, Bueno-De-Mesquita, HB, Vodickova, L, Basso, D, Obazee, O, Hackert, T, Soucek, P, Cuk, K, Kaiser, J, Sperti, C, Lovecek, M, Capurso, G, Mohelnikova-Duchonova, B, Khaw, K-T, König, A-K, Kupcinskas, J, Kaaks, R, Bambi, F, Archibugi, L, Mambrini, A, Cavestro, GM, Landi, S, Hegyi, P, Izbicki, JR, Gioffreda, D, Zambon, CF, Tavano, F, Talar-Wojnarowska, R, Jamroziak, K, Key, TJ, Fave, GD, Strobel, O, Jonaitis, L, Andriulli, A, Lawlor, RT, Pirozzi, F, Katzke, V, Valsuani, C, Vashist, YK, Brenner, H, Canzian, F, Campa, D., Matarazzi, M., Greenhalf, W., Bijlsma, M., Saum, K. -U., Pasquali, C., van Laarhoven, H., Szentesi, A., Federici, F., Vodicka, P., Funel, N., Pezzilli, R., Bueno-de-Mesquita, H. B., Vodickova, L., Basso, D., Obazee, O., Hackert, T., Soucek, P., Cuk, K., Kaiser, J., Sperti, C., Lovecek, M., Capurso, G., Mohelnikova-Duchonova, B., Khaw, K. -T., Konig, A. -K., Kupcinskas, J., Kaaks, R., Bambi, F., Archibugi, L., Mambrini, A., Cavestro, G. M., Landi, S., Hegyi, P., Izbicki, J. R., Gioffreda, D., Zambon, C. F., Tavano, F., Talar-Wojnarowska, R., Jamroziak, K., Key, T. J., Fave, G. D., Strobel, O., Jonaitis, L., Andriulli, A., Lawlor, R. T., Pirozzi, F., Katzke, V., Valsuani, C., Vashist, Y. K., Brenner, H., Canzian, F., Center of Experimental and Molecular Medicine, CCA - Cancer biology and immunology, Radiotherapy, Oncology, and AGEM - Re-generation and cancer of the digestive system
Subjects: Male, Cancer Research, pancreatic ductal adenocarcinoma, Polymorphism, Single Nucleotide, lymphocyte telomere length, genetic polymorphisms, association, Mendelian randomization, Oncology, Humans, genetic polymorphism, Lymphocytes, Telomerase, Telomere Shortening, Aged, Pancreatic Neoplasm, Ribonucleoprotein, Middle Aged, Telomere, Pancreatic Neoplasms, Europe, Ribonucleoproteins, Case-Control Studies, Female, Lymphocyte, Case-Control Studie, Carcinoma, Pancreatic Ductal, Genome-Wide Association Study, Human
Abstract: Telomere deregulation is a hallmark of cancer. Telomere length measured in lymphocytes (LTL) has been shown to be a risk marker for several cancers. For pancreatic ductal adenocarcinoma (PDAC) consensus is lacking whether risk is associated with long or short telomeres. Mendelian randomization approaches have shown that a score built from SNPs associated with LTL could be used as a robust risk marker. We explored this approach in a large scale study within the PANcreatic Disease ReseArch (PANDoRA) consortium. We analyzed 10 SNPs (ZNF676-rs409627, TERT-rs2736100, CTC1-rs3027234, DHX35-rs6028466, PXK-rs6772228, NAF1-rs7675998, ZNF208-rs8105767, OBFC1-rs9420907, ACYP2-rs11125529 and TERC-rs10936599) alone and combined in a LTL genetic score (“teloscore”, which explains 2.2% of the telomere variability) in relation to PDAC risk in 2,374 cases and 4,326 controls. We identified several associations with PDAC risk, among which the strongest were with the TERT-rs2736100 SNP (OR = 1.54; 95%CI 1.35–1.76; p = 1.54 × 10 −10 ) and a novel one with the NAF1-rs7675998 SNP (OR = 0.80; 95%CI 0.73–0.88; p = 1.87 × 10 −6 , p trend = 3.27 × 10 −7 ). The association of short LTL, measured by the teloscore, with PDAC risk reached genome-wide significance (p = 2.98 × 10 −9 for highest vs. lowest quintile; p = 1.82 × 10 −10 as a continuous variable). In conclusion, we present a novel genome-wide candidate SNP for PDAC risk (TERT-rs2736100), a completely new signal (NAF1-rs7675998) approaching genome-wide significance and we report a strong association between the teloscore and risk of pancreatic cancer, suggesting that telomeres are a potential risk factor for pancreatic cancer.
Published: 2019

3. Genome-wide association study identifies an early onset pancreatic cancer risk locus

Author: Campa, D. Gentiluomo, M. Obazee, O. Ballerini, A. Vodickova, L. Hegyi, P. Soucek, P. Brenner, H. Milanetto, A.C. Landi, S. Gao, X. Bozzato, D. Capurso, G. Tavano, F. Vashist, Y. Hackert, T. Bambi, F. Bursi, S. Oliverius, M. Gioffreda, D. Schöttker, B. Ivanauskas, A. Mohelnikova-Duchonova, B. Darvasi, E. Pezzilli, R. Małecka-Panas, E. Strobel, O. Gazouli, M. Katzke, V. Szentesi, A. Cavestro, G.M. Farkas, G., Jr. Izbicki, J.R. Moz, S. Archibugi, L. Hlavac, V. Vincze, Á. Talar-Wojnarowska, R. Rusev, B. Kupcinskas, J. Greenhalf, B. Dijk, F. Giese, N. Boggi, U. Andriulli, A. Busch, O.R. Vanella, G. Vodicka, P. Nentwich, M. Lawlor, R.T. Theodoropoulos, G.E. Jamroziak, K. Zuppardo, R.A. Moletta, L. Ginocchi, L. Kaaks, R. Neoptolemos, J.P. Lucchesi, M. Canzian, F.
Abstract: Early onset pancreatic cancer (EOPC) is a rare disease with a very high mortality rate. Almost nothing is known on the genetic susceptibility of EOPC, therefore, we performed a genome-wide association study (GWAS) to identify novel genetic variants specific for patients diagnosed with pancreatic ductal adenocarcinoma (PDAC) at younger ages. In the first phase, conducted on 821 cases with age of onset ≤60 years, of whom 198 with age of onset ≤50, and 3227 controls from PanScan I-II, we observed four SNPs (rs7155613, rs2328991, rs4891017 and rs12610094) showing an association with EOPC risk (P < 1 × 10−4). We replicated these SNPs in the PANcreatic Disease ReseArch (PANDoRA) consortium and used additional in silico data from PanScan III and PanC4. Among these four variants rs2328991 was significant in an independent set of 855 cases with age of onset ≤60 years, of whom 265 with age of onset ≤50, and 4142 controls from the PANDoRA consortium while in the in silico data, we observed no statistically significant association. However, the resulting meta-analysis supported the association (P = 1.15 × 10−4). In conclusion, we propose a novel variant rs2328991 to be involved in EOPC risk. Even though it was not possible to find a mechanistic link between the variant and the function, the association is supported by a solid statistical significance obtained in the largest study on EOPC genetics present so far in the literature. © 2020 UICC
Published: 2020

4. Germline BRCA2 K3326X and CHEK2 I157T mutations increase risk for sporadic pancreatic ductal adenocarcinoma

Author: Obazee, O., Archibugi, L., Andriulli, A., Soucek, P., Malecka-Panas, E., Ivanauskas, A., Johnson, T., Gazouli, M., Pausch, T., Lawlor, R. T., Cavestro, G. M., Milanetto, A. C., Di Leo, M., Pasquali, C., Hegyi, P., Szentesi, A., Radu, C. E., Gheorghe, C., Theodoropoulos, G. E., Bergmann, F., Brenner, H., Vodickova, L., Katzke, V., Campa, D., Strobel, O., Kaiser, J., Pezzilli, R., Federici, F., Mohelnikova-Duchonova, B., Boggi, U., Lemstrova, R., Johansen, J. S., Bojesen, S. E., Chen, I., Jensen, B. V., Capurso, G., Pazienza, V., Dervenis, C., Sperti, C., Mambrini, A., Hackert, T., Kaaks, R., Basso, D., Talar-Wojnarowska, R., Maiello, E., Izbicki, J. R., Cuk, K., Saum, K. U., Cantore, M., Kupcinskas, J., Palmieri, O., Delle Fave, G., Landi, S., Salvia, R., Fogar, P., Vashist, Y. K., Scarpa, A., Vodicka, P., Tjaden, C., Iskierka-Jazdzewska, E., Canzian, F., Obazee, O., Archibugi, L., Andriulli, A., Soucek, P., Malecka-Panas, E., Ivanauskas, A., Johnson, T., Gazouli, M., Pausch, T., Lawlor, R. T., Cavestro, G. M., Milanetto, A. C., Di Leo, M., Pasquali, C., Hegyi, P., Szentesi, A., Radu, C. E., Gheorghe, C., Theodoropoulos, G. E., Bergmann, F., Brenner, H., Vodickova, L., Katzke, V., Campa, D., Strobel, O., Kaiser, J., Pezzilli, R., Federici, F., Mohelnikova-Duchonova, B., Boggi, U., Lemstrova, R., Johansen, J. S., Bojesen, S. E., Chen, I., Jensen, B. V., Capurso, G., Pazienza, V., Dervenis, C., Sperti, C., Mambrini, A., Hackert, T., Kaaks, R., Basso, D., Talar-Wojnarowska, R., Maiello, E., Izbicki, J. R., Cuk, K., Saum, K. U., Cantore, M., Kupcinskas, J., Palmieri, O., Delle Fave, G., Landi, S., Salvia, R., Fogar, P., Vashist, Y. K., Scarpa, A., Vodicka, P., Tjaden, C., Iskierka-Jazdzewska, E., and Canzian, F.
Subjects: Male, Cancer Research, pancreatic cancer, Genes, BRCA2, I157T, Polymorphism, Single Nucleotide, Humans, Genetic Predisposition to Disease, Germ-Line Mutation, Aged, BRCA2 Protein, K3326X, PANDoRA consortium, rs11571833, rs17879961, Oncology, Pancreatic cancer, Middle Aged, Pancreatic Neoplasms, Checkpoint Kinase 2, Case-Control Studies, Female, Carcinoma, Pancreatic Ductal
Abstract: Rare truncating BRCA2 K3326X (rs11571833) and pathogenic CHEK2 I157T (rs17879961) variants have previously been implicated in familial pancreatic ductal adenocarcinoma (PDAC), but not in sporadic cases. The effect of both mutations in important DNA repair genes on sporadic PDAC risk may shed light on the genetic architecture of this disease. Both mutations were genotyped in germline DNA from 2,935 sporadic PDAC cases and 5,626 control subjects within the PANcreatic Disease ReseArch (PANDoRA) consortium. Risk estimates were evaluated using multivariate unconditional logistic regression with adjustment for possible confounders such as sex, age and country of origin. Statistical analyses were two-sided with p values
Published: 2018

5. Germline BRCA2 K3326X and CHEK2 I157T mutations increase risk for sporadic pancreatic ductal adenocarcinoma

Author: Obazee, O. Archibugi, L. Andriulli, A. Soucek, P. Małecka-Panas, E. Ivanauskas, A. Johnson, T. Gazouli, M. Pausch, T. Lawlor, R.T. Cavestro, G.M. Milanetto, A.C. Di Leo, M. Pasquali, C. Hegyi, P. Szentesi, A. Radu, C.E. Gheorghe, C. Theodoropoulos, G.E. Bergmann, F. Brenner, H. Vodickova, L. Katzke, V. Campa, D. Strobel, O. Kaiser, J. Pezzilli, R. Federici, F. Mohelnikova-Duchonova, B. Boggi, U. Lemstrova, R. Johansen, J.S. Bojesen, S.E. Chen, I. Jensen, B.V. Capurso, G. Pazienza, V. Dervenis, C. Sperti, C. Mambrini, A. Hackert, T. Kaaks, R. Basso, D. Talar-Wojnarowska, R. Maiello, E. Izbicki, J.R. Cuk, K. Saum, K.U. Cantore, M. Kupcinskas, J. Palmieri, O. Delle Fave, G. Landi, S. Salvia, R. Fogar, P. Vashist, Y.K. Scarpa, A. Vodicka, P. Tjaden, C. Iskierka-Jazdzewska, E. Canzian, F.
Abstract: Rare truncating BRCA2 K3326X (rs11571833) and pathogenic CHEK2 I157T (rs17879961) variants have previously been implicated in familial pancreatic ductal adenocarcinoma (PDAC), but not in sporadic cases. The effect of both mutations in important DNA repair genes on sporadic PDAC risk may shed light on the genetic architecture of this disease. Both mutations were genotyped in germline DNA from 2,935 sporadic PDAC cases and 5,626 control subjects within the PANcreatic Disease ReseArch (PANDoRA) consortium. Risk estimates were evaluated using multivariate unconditional logistic regression with adjustment for possible confounders such as sex, age and country of origin. Statistical analyses were two-sided with p values
Published: 2019

6. A multifactorial score for pancreatic ductal adenocarcinoma risk prediction

Author: Gentiluomo, M., Galeotti, A. A., Rizzato, C., Obazee, O., Neoptolemos, J. P., Pasquali, C., Nentwick, M., Cavestro, G. M., Pezzilli, R., Greenhalf, W., Holleczek, B., Shroeder, C., Shottker, B., Ivanauskas, A., Ginocchi, L., Key, T. J., Hegyi, P., Archibugi, L., Darvasi, E., Basso, D., Sperti, C., Bijlisma, M. F., Palmieri, G., Hlavac, V., Talar-Wojnarowska, R., Mohelnikova – Duchonova, B., Hackert, T., Vahist, Y., Strouhal, O., van Laarhoven, C., Tavano, F., Lovecek, M., Dervenis, C., Izbeki, F., Padoan, A., Malencka-Panas, E., Maiello, E., Vanella, G., Capurso, G., Izbicki, J. R., Theodoropulos, G. E., Jamroziak, K., Katzke, V., Kaaks, R., Mambrini, A., Papanikolaou, I. S., Szentesi, A., Kupcinskas, J., Bursi, S., Costello, E., Boggi, U., Milanetto, A. C., Landi, S., Gazouli, M., Vodickova, L., Soucek, P., Gioffreda, D., Gemignani, F., Brenner, H., Strobel, O., Bukler, M. W., Vodicka, P., Paiella, S, Canzian, F., and Campa, D. :.
Published: 2019

7. Genome-wide association study identifies an early onset pancreatic cancer risk locus

Author: Gentiluomo, M., Obazee, O., Ballerini, A., Vodickova, L., Hegyi, P., Soucek, P., Brenner, H., Milanetto, A. C., Landi, S., Gao, X., Bozzato, D., Capurso, G., Tavano, F., Vashist, Y., Hackert, T., Bambi, F., Bursi, S., Oliverius, M., Gioffreda, D., Schöttker, B., Ivanauskas, A., Mohelnikova-Duchonova, B., Darvasi, E., Pezzilli, R., Małecka-Panas, E., Strobel, O., Gazouli, M., Katzke, V., Szentesi, A., Cavestro, G. M., Farkas, G. Jr., Izbicki, J. R., Moz, S., Archibugi, L., Hlavac, V., Vincze, A., Talar-Wojnarowska, R., Borislav, R., Kupcinskas, J., Greenhalf, B., Dijk, F., Giese, N., Boggi, U., Andriulli, A., Busch, O. R., Vanella, G., Vodicka, P., Nentwich, M., Lawlor, R. T., Theodoropoulos, G. E., Jamroziak, K., Zuppardo, R. A., Moletta, L., Ginocchi, L., Kaaks, R., Neoptolemos, J. P., Lucchesi, M., Canzian, F., and Campa, D.
Published: 2019

8. Genetic variability of the ABCC2 gene and overall survival in pancreatic cancer

Author: Gentiluomo, M., Galeotti, A., Pezzilli, R., Boggi, U., Capurso, G., Małecka-Panas, E., Kupcinskas, J., Büchler, M., Andriulli, A., Greenhalf, W., Neoptolemos, J. P., Mambrini, A., Scarpa, A., Soucek, P., Lovecek, M., Puchalt García, P., Obazee, O., Pasquali, C., Busch, O., Izbicki, J., Vashist, J. K., Cavestro, G. M., Hegyi, P., Canzian, F., and Campa, D
Published: 2018

9. Corrigendum: Common genetic variants associated with pancreatic adenocarcinoma may also modify risk of pancreatic neuroendocrine neoplasms [Carcinogenesis, 39, 3, (2018), (360-367)] DOI: 10.1093/carcin/bgx150

Author: Obazee, O. Capurso, G. Tavano, F. Archibugi, L. De Bonis, A. Greenhalf, W. Key, T. Pasquali, C. Milanetto, A.C. Hackert, T. Fogar, P. Lico, V. Dervenis, C. Lawlor, R.T. Landoni, L. Gazouli, M. Zambon, C.F. Funel, N. Strobel, O. Jamroziak, K. Cantu, C. Malecka-Panas, E. Landi, S. Neoptolemos, J.P. Basso, D. Talar-Wojnarowska, R. Rinzivillo, M. Andriulli, A. Canzian, F. Campa, D.
Subjects: GeneralLiterature_REFERENCE(e.g.,dictionaries,encyclopedias,glossaries), GeneralLiterature_MISCELLANEOUS
Abstract: In the originally published version of this article, the institutional affiliations of some authors were listed incorrectly. The correct affiliations are as listed above. This has been corrected online. The authors wish to apologize for this error. © The Author(s) 2018. Published by Oxford University Press. All rights reserved.
Published: 2018

10. Genome-wide meta-analysis identifies five new susceptibility loci for pancreatic cancer

Author: Klein, A.P. Wolpin, B.M. Risch, H.A. Stolzenberg-Solomon, R.Z. Mocci, E. Zhang, M. Canzian, F. Childs, E.J. Hoskins, J.W. Jermusyk, A. Zhong, J. Chen, F. Albanes, D. Andreotti, G. Arslan, A.A. Babic, A. Bamlet, W.R. Beane-Freeman, L. Berndt, S.I. Blackford, A. Borges, M. Borgida, A. Bracci, P.M. Brais, L. Brennan, P. Brenner, H. Bueno-De-Mesquita, B. Buring, J. Campa, D. Capurso, G. Cavestro, G.M. Chaffee, K.G. Chung, C.C. Cleary, S. Cotterchio, M. Dijk, F. Duell, E.J. Foretova, L. Fuchs, C. Funel, N. Gallinger, S. Gaziano, J.M.M. Gazouli, M. Giles, G.G. Giovannucci, E. Goggins, M. Goodman, G.E. Goodman, P.J. Hackert, T. Haiman, C. Hartge, P. Hasan, M. Hegyi, P. Helzlsouer, K.J. Herman, J. Holcatova, I. Holly, E.A. Hoover, R. Hung, R.J. Jacobs, E.J. Jamroziak, K. Janout, V. Kaaks, R. Khaw, K.-T. Klein, E.A. Kogevinas, M. Kooperberg, C. Kulke, M.H. Kupcinskas, J. Kurtz, R.J. Laheru, D. Landi, S. Lawlor, R.T. Lee, I.-M. Lemarchand, L. Lu, L. Malats, N. Mambrini, A. Mannisto, S. Milne, R.L. Mohelníková-Duchoňová, B. Neale, R.E. Neoptolemos, J.P. Oberg, A.L. Olson, S.H. Orlow, I. Pasquali, C. Patel, A.V. Peters, U. Pezzilli, R. Porta, M. Real, F.X. Rothman, N. Scelo, G. Sesso, H.D. Severi, G. Shu, X.-O. Silverman, D. Smith, J.P. Soucek, P. Sund, M. Talar-Wojnarowska, R. Tavano, F. Thornquist, M.D. Tobias, G.S. Van Den Eeden, S.K. Vashist, Y. Visvanathan, K. Vodicka, P. Wactawski-Wende, J. Wang, Z. Wentzensen, N. White, E. Yu, H. Yu, K. Zeleniuch-Jacquotte, A. Zheng, W. Kraft, P. Li, D. Chanock, S. Obazee, O. Petersen, G.M. Amundadottir, L.T.
Abstract: In 2020, 146,063 deaths due to pancreatic cancer are estimated to occur in Europe and the United States combined. To identify common susceptibility alleles, we performed the largest pancreatic cancer GWAS to date, including 9040 patients and 12,496 controls of European ancestry from the Pancreatic Cancer Cohort Consortium (PanScan) and the Pancreatic Cancer Case-Control Consortium (PanC4). Here, we find significant evidence of a novel association at rs78417682 (7p12/TNS3, P = 4.35 × 10-8). Replication of 10 promising signals in up to 2737 patients and 4752 controls from the PANcreatic Disease ReseArch (PANDoRA) consortium yields new genome-wide significant loci: Rs13303010 at 1p36.33 (NOC2L, P = 8.36 × 10-14), rs2941471 at 8q21.11 (HNF4G, P = 6.60 × 10-10), rs4795218 at 17q12 (HNF1B, P = 1.32 × 10-8), and rs1517037 at 18q21.32 (GRP, P = 3.28 × 10-8). rs78417682 is not statistically significantly associated with pancreatic cancer in PANDoRA. Expression quantitative trait locus analysis in three independent pancreatic data sets provides molecular support of NOC2L as a pancreatic cancer susceptibility gene. © 2018 The Author(s).
Published: 2018

11. Common genetic variants associated with pancreatic adenocarcinoma may also modify risk of pancreatic neuroendocrine neoplasms

Author: Obazee, O. Capurso, G. Tavano, F. Archibugi, L. Bonis, A.D. Greenhalf, W. Key, T. Pasquali, C. Milanetto, A.C. Hackert, T. Fogar, P. Liço, V. Dervenis, C. Lawlor, R.T. Landoni, L. Gazouli, M. Zambon, C.F. Funel, N. Strobel, O. Jamroziak, K. Cantù, C. Malecka-Panas, E. Landi, S. Neoptolemos, J.P. Basso, D. Talar-Wojnarowska, R. Rinzivillo, M. Andriulli, A. Canzian, F. Campa, D.
Abstract: Pancreatic neuroendocrine neoplasms (pNEN) account for less than 5% of all pancreatic neoplasms and genetic association studies on susceptibility to the disease are limited. We sought to identify possible overlap of genetic susceptibility loci between pancreatic ductal adenocarcinoma (PDAC) and pNEN; therefore, PDAC susceptibility variants (n = 23) from Caucasian genome-wide association studies (GWAS) were genotyped in 369 pNEN cases and 3277 controls from the PANcreatic Disease ReseArch (PANDoRA) consortium to evaluate the odds associated with pNEN risk, disease onset and tumor characteristics. Main effect analyses showed four PDAC susceptibility variants-rs9854771, rs1561927, rs9543325 and rs10919791 to be associated with pNEN risk. Subsequently, only associations with rs9543325, rs10919791 and rs1561927 were noteworthy with false positive report probability (FPRP) tests. Stratified analyses considering age at onset (50-year threshold), showed rs2736098, rs16986825 and rs9854771 to be associated with risk of developing pNEN at a younger age. Stratified analyses also showed some single nucleotide polymorphisms to be associated with different degrees of tumor grade, metastatic potential and functionality. Our results identify known GWAS PDAC susceptibility loci, which may also be involved in sporadic pNEN etiology and suggest that some genetic mechanisms governing pathogenesis of these two entities may be similar, with few of these loci being more influential in younger cases or tumor subtypes. © The Author(s) 2018. Published by Oxford University Press. All rights reserved.
Published: 2018

12. Germline BRCA2 K3326X and CHEK2 I157T mutations increase risk for sporadic pancreatic ductal adenocarcinoma

Author: Obazee, O., primary, Archibugi, L., additional, Andriulli, A., additional, Soucek, P., additional, Małecka-Panas, E., additional, Ivanauskas, A., additional, Johnson, T., additional, Gazouli, M., additional, Pausch, T., additional, Lawlor, R. T., additional, Cavestro, G. M., additional, Milanetto, A. C., additional, Di Leo, M., additional, Pasquali, C., additional, Hegyi, P., additional, Szentesi, A., additional, Radu, C. E., additional, Gheorghe, C., additional, Theodoropoulos, G. E., additional, Bergmann, F., additional, Brenner, H., additional, Vodickova, L., additional, Katzke, V., additional, Campa, D., additional, Strobel, O., additional, Kaiser, J., additional, Pezzilli, R., additional, Federici, F., additional, Mohelnikova-Duchonova, B., additional, Boggi, U., additional, Lemstrova, R., additional, Johansen, J. S., additional, Bojesen, S. E., additional, Chen, I., additional, Jensen, B. V., additional, Capurso, G., additional, Pazienza, V., additional, Dervenis, C., additional, Sperti, C., additional, Mambrini, A., additional, Hackert, T., additional, Kaaks, R., additional, Basso, D., additional, Talar-Wojnarowska, R., additional, Maiello, E., additional, Izbicki, J. R., additional, Cuk, K., additional, Saum, K. U., additional, Cantore, M., additional, Kupcinskas, J., additional, Palmieri, O., additional, Delle Fave, G., additional, Landi, S., additional, Salvia, R., additional, Fogar, P., additional, Vashist, Y. K., additional, Scarpa, A., additional, Vodicka, P., additional, Tjaden, C., additional, Iskierka-Jazdzewska, E., additional, and Canzian, F., additional
Published: 2019
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13. Genetic determinants of telomere length and risk of pancreatic cancer: a PANDoRA study

Author: Campa, D, Pezzilli, R, Boggi, U, Capurso, G, Talar-Wojnarowska, R, Kupcinskas, J, Hackert, T, Vodicka, P, Cavestro, Gm, Khaw, Kt, Key, T, Landi, S, Tavano, F, Gentiluomo, M, Costello, E, Mambrini, A, Lawlor, Rt, Soucek, P, Kaaks, R, Milanetto, A. C., Obazee, O, Dijk, F, Vashist, Yk, Hegyi, P, and Canzian, F
Published: 2017

14. Do pancreatic adenocarcinoma and neuroendocrine neoplasms share genetic susceptability a PANDoRA study

Author: Canzian, F., Capurso, G., Andriulli, A., Neoptolemos, J. P., Malenka Panas, E., Kaaks, R., Gazouli, M., Strobel, O., Scarpa, A., Pasquali, Claudio, Landi, S., Boggi, U., Khaw, K. T., Key, T. J., Campa, D., and Obazee, O.
Published: 2017

15. Three new pancreatic cancer susceptibility signals identified on chromosomes 1q32.1, 5p15.33 and 8q24.21

Author: Zhang, M. Wang, Z. Obazee, O. Jia, J. Childs, E.J. Hoskins, J. Figlioli, G. Mocci, E. Collins, I. Chung, C.C. Hautman, C. Arslan, A.A. Beane-Freeman, L. Bracci, P.M. Buring, J. Duell, E.J. Gallinger, S. Giles, G.G. Goodman, G.E. Goodman, P.J. Kamineni, A. Kolonel, L.N. Kulke, M.H. Malats, N. Olson, S.H. Sesso, H.D. Visvanathan, K. White, E. Zheng, W. Abnet, C.C. Albanes, D. Andreotti, G. Brais, L. Bas Bueno-de-Mesquita, H. Basso, D. Berndt, S.I. Boutron-Ruault, M.-C. Bijlsma, M.F. Brenner, H. Burdette, L. Campa, D. Caporaso, N.E. Capurso, G. Cavestro, G.M. Cotterchio, M. Costello, E. Elena, J. Boggi, U. Michael Gaziano, J. Gazouli, M. Giovannucci, E.L. Goggins, M. Gross, M. Haiman, C.A. Hassan, M. Helzlsouer, K.J. Hu, N. Hunter, D.J. Iskierka-Jazdzewska, E. Jenab, M. Kaaks, R. Key, T.J. Khaw, K.-T. Klein, E.A. Kogevinas, M. Krogh, V. Kupcinskas, J. Kurtz, R.C. Landi, M.T. Landi, S. Marchand, L.L. Mambrini, A. Mannisto, S. Milne, R.L. Neale, R.E. Oberg, A.L. Panico, S. Patel, A.V. Peeters, P.H.M. Peters, U. Pezzilli, R. Porta, M. Purdue, M. Ramón Quiros, J. Riboli, E. Rothman, N. Scarpa, A. Scelo, G. Shu, X.-O. Silverman, D.T. Soucek, P. Strobel, O. Sund, M. Malecka-Panas, E. Taylor, P.R. Tavano, F. Travis, R.C. Thornquist, M. Tjønneland, A. Tobias, G.S. Trichopoulos, D. Vashist, Y. Vodicka, P. Wactawski-Wende, J. Wentzensen, N. Yu, H. Yu, K. Zeleniuch-Jacquotte, A. Kooperberg, C. Risch, H.A. Jacobs, E.J. Li, D. Fuchs, C. Hoover, R. Hartge, P. Chanock, S.J. Petersen, G.M. Stolzenberg-Solomon, R.S. Wolpin, B.M. Kraft, P. Klein, A.P. Canzian, F. Amundadottir, L.T.
Abstract: Genome-wide association studies (GWAS) have identified common pancreatic cancer susceptibility variants at 13 chromosomal loci in individuals of European descent. To identify new susceptibility variants, we performed imputation based on 1000 Genomes (1000G) Project data and association analysis using 5,107 case and 8,845 control subjects from 27 cohort and case-control studies that participated in the PanScan I-III GWAS. This analysis, in combination with a two-staged replication in an additional 6,076 case and 7,555 control subjects from the PANcreatic Disease ReseArch (PANDoRA) and Pancreatic Cancer Case-Control (PanC4) Consortia uncovered 3 new pancreatic cancer risk signals marked by single nucleotide polymorphisms (SNPs) rs2816938 at chromosome 1q32.1 (per allele odds ratio (OR) = 1.20, P = 4.88x10-15), rs10094872 at 8q24.21 (OR = 1.15, P = 3.22x10-9) and rs35226131 at 5p15.33 (OR = 0.71, P = 1.70x10-8). These SNPs represent independent risk variants at previously identified pancreatic cancer risk loci on chr1q32.1 (NR5A2), chr8q24.21 (MYC) and chr5p15.33 (CLPTM1L-TERT) as per analyses conditioned on previously reported susceptibility variants. We assessed expression of candidate genes at the three risk loci in histologically normal (n = 10) and tumor (n = 8) derived pancreatic tissue samples and observed a marked reduction of NR5A2 expression (chr1q32.1) in the tumors (fold change -7.6, P = 5.7x10-8). This finding was validated in a second set of paired (n = 20) histologically normal and tumor derived pancreatic tissue samples (average fold change for three NR5A2 isoforms -31.3 to -95.7, P = 7.5x10-4-2.0x10-3). Our study has identified new susceptibility variants independently conferring pancreatic cancer risk that merit functional follow-up to identify target genes and explain the underlying biology.
Published: 2016

16. Polygenic and multifactorial scores for pancreatic ductal adenocarcinoma risk prediction

Author: John P. Neoptolemos, Markus W. Büchler, Jakob R. Izbicki, Ben Schöttker, Cosmeri Rizzato, Cornelia Schroeder, Salvatore Paiella, Hanneke W. M. van Laarhoven, William Greenhalf, Simona Bursi, Renata Talar-Wojnarowska, Christos Dervenis, Ludmila Vodickova, Francesca Tavano, Giulia Martina Cavestro, Thilo Hackert, Claudio Pasquali, Ewa Małecka-Panas, Gabriele Capurso, Andrea Mambrini, Daniele Campa, Andrea Padoan, Ioannis S. Papanikolaou, Raffaele Pezzilli, Péter Hegyi, Beatrice Mohelnikova-Duchonova, Federica Gemignani, Michael F. Nentwich, Pavel Vodicka, Stefano Landi, Richárd Szmola, Anna Caterina Milanetto, Eithne Costello, Rudolf Kaaks, Laura Ginocchi, Bernd Holleczek, Erika Darvasi, Verena Katzke, Evaristo Maiello, Manuel Gentiluomo, Ondrej Strouhal, Orazio Palmieri, Juozas Kupcinskas, Alice Alessandra Galeotti, Viktor Hlavac, George Theodoropoulos, Audrius Ivanauskas, Maria Gazouli, Ferenc Izbéki, Federico Canzian, Oliver Strobel, Ofure Obazee, Martin Lovecek, Timothy J. Key, Domenica Gioffreda, Pavel Soucek, Ugo Boggi, Krzysztof Jamroziak, Cosimo Sperti, Maarten F. Bijlsma, Yogesh K. Vashist, Andrea Szentesi, Hermann Brenner, Livia Archibugi, Giuseppe Vanella, Daniela Basso, Radiotherapy, Center of Experimental and Molecular Medicine, CCA - Cancer Treatment and Quality of Life, Oncology, AGEM - Amsterdam Gastroenterology Endocrinology Metabolism, Galeotti, A. A., Gentiluomo, M., Rizzato, C., Obazee, O., Neoptolemos, J. P., Pasquali, C., Nentwich, M., Cavestro, G. M., Pezzilli, R., Greenhalf, W., Holleczek, B., Schroeder, C., Schottker, B., Ivanauskas, A., Ginocchi, L., Key, T. J., Hegyi, P., Archibugi, L., Darvasi, E., Basso, D., Sperti, C., Bijlsma, M. F., Palmieri, O., Hlavac, V., Talar-Wojnarowska, R., Mohelnikova-Duchonova, B., Hackert, T., Vashist, Y., Strouhal, O., Van Laarhoven, H., Tavano, F., Lovecek, M., Dervenis, C., Izbeki, F., Padoan, A., Malecka-Panas, E., Maiello, E., Vanella, G., Capurso, G., Izbicki, J. R., Theodoropoulos, G. E., Jamroziak, K., Katzke, V., Kaaks, R., Mambrini, A., Papanikolaou, I. S., Szmola, R., Szentesi, A., Kupcinskas, J., Bursi, S., Costello, E., Boggi, U., Milanetto, A. C., Landi, S., Gazouli, M., Vodickova, L., Soucek, P., Gioffreda, D., Gemignani, F., Brenner, H., Strobel, O., Buchler, M., Vodicka, P., Paiella, S., Canzian, F., and Campa, D.
Subjects: 0301 basic medicine, Oncology, Male, medicine.medical_specialty, Multifactorial Inheritance, Pancreatic disease, genetic epidemiology, Population, Single-nucleotide polymorphism, Disease, pancreas and biliary tract, Polymorphism, Single Nucleotide, Risk Assessment, ABO Blood-Group System, 03 medical and health sciences, 0302 clinical medicine, Gene Frequency, Pancreatic cancer, Internal medicine, Genetics, medicine, oncology, Humans, education, Genetics (clinical), Alleles, Early Detection of Cancer, Genetic association, education.field_of_study, business.industry, medicine.disease, Pancreatic Neoplasms, 030104 developmental biology, Genetic epidemiology, 030220 oncology & carcinogenesis, Cohort, Female, business, Carcinoma, Pancreatic Ductal
Abstract: BackgroundMost cases of pancreatic ductal adenocarcinoma (PDAC) are asymptomatic in early stages, and the disease is typically diagnosed in advanced phases, resulting in very high mortality. Tools to identify individuals at high risk of developing PDAC would be useful to improve chances of early detection.ObjectiveWe generated a polygenic risk score (PRS) for PDAC risk prediction, combining the effect of known risk SNPs, and carried out an exploratory analysis of a multifactorial score.MethodsWe tested the associations of the individual known risk SNPs on up to 2851 PDAC cases and 4810 controls of European origin from the PANcreatic Disease ReseArch (PANDoRA) consortium. Thirty risk SNPs were included in a PRS, which was computed on the subset of subjects that had 100% call rate, consisting of 839 cases and 2040 controls in PANDoRA and 6420 cases and 4889 controls from the previously published Pancreatic Cancer Cohort Consortium I–III and Pancreatic Cancer Case-Control Consortium genome-wide association studies. Additional exploratory multifactorial scores were constructed by complementing the genetic score with smoking and diabetes.ResultsThe scores were associated with increased PDAC risk and reached high statistical significance (OR=2.70, 95% CI 1.99 to 3.68, p=2.54×10−10 highest vs lowest quintile of the weighted PRS, and OR=14.37, 95% CI 5.57 to 37.09, p=3.64×10−8, highest vs lowest quintile of the weighted multifactorial score).ConclusionWe found a highly significant association between a PRS and PDAC risk, which explains more than individual SNPs and is a step forward in the direction of the construction of a tool for risk stratification in the population.
Published: 2020

17. Genome-wide association study identifies an early onset pancreatic cancer risk locus

Author: Verena Katzke, Jakob R. Izbicki, Francesca Tavano, Rita T. Lawlor, Thilo Hackert, Raffaella Alessia Zuppardo, Giulia Martina Cavestro, Federico Canzian, Frederike Dijk, Martin Oliverius, George Theodoropoulos, Pavel Soucek, Manuel Gentiluomo, Rudolf Kaaks, Erika Darvasi, Yogesh K. Vashist, Bill Greenhalf, Juozas Kupcinskas, Maurizio Lucchesi, Borislav Rusev, Andrea Szentesi, Gabriele Capurso, Ewa Małecka-Panas, Lucia Moletta, Beatrice Mohelnikova-Duchonova, Franco Bambi, Ugo Boggi, Alba Ballerini, Krzysztof Jamroziak, Ben Schöttker, Simona Bursi, Raffaele Pezzilli, Gyula Farkas, Dania Bozzato, Áron Vincze, Stefano Landi, Anna Caterina Milanetto, Péter Hegyi, Michael F. Nentwich, Laura Ginocchi, Pavel Vodicka, Stefania Moz, Ludmila Vodickova, Hermann Brenner, Olivier R. Busch, Viktor Hlavac, Audrius Ivanauskas, John P. Neoptolemos, Domenica Gioffreda, Ofure Obazee, Livia Archibugi, Nathalia A. Giese, Giuseppe Vanella, Xin Gao, Renata Talar-Wojnarowska, Angelo Andriulli, Oliver Strobel, Daniele Campa, Maria Gazouli, Pathology, CCA - Cancer biology and immunology, Surgery, AGEM - Digestive immunity, AGEM - Endocrinology, metabolism and nutrition, AGEM - Re-generation and cancer of the digestive system, AGEM - Amsterdam Gastroenterology Endocrinology Metabolism, Campa, D., Gentiluomo, M., Obazee, O., Ballerini, A., Vodickova, L., Hegyi, P., Soucek, P., Brenner, H., Milanetto, A. C., Landi, S., Gao, X., Bozzato, D., Capurso, G., Tavano, F., Vashist, Y., Hackert, T., Bambi, F., Bursi, S., Oliverius, M., Gioffreda, D., Schottker, B., Ivanauskas, A., Mohelnikova-Duchonova, B., Darvasi, E., Pezzilli, R., Malecka-Panas, E., Strobel, O., Gazouli, M., Katzke, V., Szentesi, A., Cavestro, G. M., Farkas, G., Izbicki, J. R., Moz, S., Archibugi, L., Hlavac, V., Vincze, A., Talar-Wojnarowska, R., Rusev, B., Kupcinskas, J., Greenhalf, B., Dijk, F., Giese, N., Boggi, U., Andriulli, A., Busch, O. R., Vanella, G., Vodicka, P., Nentwich, M., Lawlor, R. T., Theodoropoulos, G. E., Jamroziak, K., Zuppardo, R. A., Moletta, L., Ginocchi, L., Kaaks, R., Neoptolemos, J. P., Lucchesi, M., and Canzian, F.
Subjects: Oncology, Male, Cancer Research, medicine.medical_specialty, Pancreatic disease, pancreatic cancer, early onset, Single-nucleotide polymorphism, Genome-wide association study, very early onset pancreatic cancer, Polymorphism, Single Nucleotide, 03 medical and health sciences, single nucleotide polymorphisms, 0302 clinical medicine, Risk Factors, Pancreatic cancer, Internal medicine, Genetic predisposition, Medicine, Humans, Genetic Predisposition to Disease, Genetic variability, Pancreas, Genetic association, genome-wide association study, business.industry, Middle Aged, medicine.disease, Pancreatic Neoplasms, 030220 oncology & carcinogenesis, Case-Control Studies, Female, Age of onset, business, Carcinoma, Pancreatic Ductal
Abstract: Early onset pancreatic cancer (EOPC) is a rare disease with a very high mortality rate. Almost nothing is known on the genetic susceptibility of EOPC, therefore we performed a genome-wide association study (GWAS) to identify novel genetic variants specific for patients diagnosed with pancreatic ductal adenocarcinoma (PDAC) at younger ages. In the first phase, conducted on 821 cases with age of onset ≤60 years, of whom 198 with age of onset ≤50, and 3227 controls from PanScan I-II, we observed four SNPs (rs7155613, rs2328991, rs4891017 and rs12610094) showing an association with EOPC risk (P < 1x10-4 ). We replicated these SNPs in the PANcreatic Disease ReseArch (PANDoRA) consortium and used additional in silico data from PanScan III and PanC4. Among these four variants rs2328991 was significant in an independent set of 855 cases with age of onset ≤60 years, of whom 265 with age of onset≤50, and 4142 controls from the PANDoRA consortium while in the in silico data we observed no statistically significant association. However, the resulting meta-analysis supported the association (P = 1.15x10-4 ). In conclusion we propose a novel variant rs2328991 to be involved in EOPC risk. Even though it was not possible to find a mechanistic link between the variant and the function, the association is supported by a solid statistical significance obtained in the largest study on EOPC genetics present so far in the literature. This article is protected by copyright. All rights reserved.
Published: 2020

18. Three new pancreatic cancer susceptibility signals identified on chromosomes 1q32.1, 5p15.33 and 8q24.21

Author: Anne Tjønneland, Jason W. Hoskins, Kala Visvanathan, Yogesh K. Vashist, Dimitrios Trichopoulos, Matthew H. Kulke, Ruth C. Travis, Charles S. Fuchs, Herbert Yu, Kai Yu, Phyllis J. Goodman, Michael Goggins, Jean Wactawski-Wende, Laurie Burdette, Joanne W. Elena, Andrea Mambrini, Petra H.M. Peeters, H. Bas Bueno-de-Mesquita, Maria Teresa Landi, Ulrike Peters, Mingfeng Zhang, Laurence N. Kolonel, Hermann Brenner, Elżbieta Iskierka-Jażdżewska, Robert C. Kurtz, Stephen J. Chanock, Marie-Christine Boutron-Ruault, Ann L. Oberg, Elio Riboli, Maarten F. Bijlsma, Eric J. Jacobs, Manolis Kogevinas, Evelina Mocci, Steven Gallinger, Jinping Jia, Mark P. Purdue, Raffaele Pezzilli, Harvey A. Risch, Demetrius Albanes, Irene Collins, Maria Gazouli, Michelle Cotterchio, Oliver Strobel, Erica J. Childs, Charles C. Chung, Geoffrey S. Tobias, J. Ramón Quirós, Núria Malats, Robert N. Hoover, Pavel Vodicka, Brian M. Wolpin, Ugo Boggi, Patricia Hartge, Gloria M. Petersen, Peter Kraft, Christopher Hautman, Gary E. Goodman, Manal Hassan, Donghui Li, Howard D. Sesso, Malin Sund, Julie E. Buring, Loic Le Marchand, Wei Zheng, Xiao-Ou Shu, Ewa Małecka-Panas, Pavel Soucek, Salvatore Panico, Nicolas Wentzensen, Graham G. Giles, Alpa V. Patel, Daniele Campa, Myron D. Gross, Ghislaine Scelo, J. Michael Gaziano, Juozas Kupcinskas, Debra T. Silverman, Laufey T. Amundadottir, Rachael S. Stolzenberg-Solomon, Neil E. Caporaso, Mazda Jenab, Sara H. Olson, Stefano Landi, Giulia Martina Cavestro, Aruna Kamineni, Laura Beane-Freeman, Roger L. Milne, Rachel E. Neale, Aldo Scarpa, Kathy J. Helzlsouer, Miquel Porta, Emily White, Eric J. Duell, Paige M. Bracci, Nan Hu, Federico Canzian, Eric A. Klein, Gabriele Capurso, Anne Zeleniuch-Jacquotte, Eithne Costello, David J. Hunter, Rudolf Kaaks, Sonja I. Berndt, Kay-Tee Khaw, Nathaniel Rothman, Christian C. Abnet, Francesca Tavano, Christopher A. Haiman, Zhaoming Wang, Ofure Obazee, Alan A. Arslan, Edward Giovannucci, Alison P. Klein, Daniela Basso, Charles Kooperberg, Philip R. Taylor, Satu Männistö, Timothy J. Key, Mark D. Thornquist, Gabriella Andreotti, Lauren K. Brais, Gisella Figlioli, Vittorio Krogh, University Medical Center Utrecht, Imperial College Trust, Cancer Research UK, Medical Research Council UK (MRC), National Institute for Health Research (NIHR), Cancer Research UK (Reino Unido), Medical Research Council (Reino Unido), National Institute for Health Research (Reino Unido), Zhang, Mingfeng, Wang, Zhaoming, Obazee, Ofure, Jia, Jinping, Childs, Erica J, Hoskins, Jason, Figlioli, Gisella, Mocci, Evelina, Collins, Irene, Chung, Charles C, Hautman, Christopher, Arslan, Alan A, Beane Freeman, Laura, Bracci, Paige M, Buring, Julie, Duell, Eric J, Gallinger, Steven, Giles, Graham G, Goodman, Gary E, Goodman, Phyllis J, Kamineni, Aruna, Kolonel, Laurence N, Kulke, Matthew H, Malats, Núria, Olson, Sara H, Sesso, Howard D, Visvanathan, Kala, White, Emily, Zheng, Wei, Abnet, Christian C, Albanes, Demetriu, Andreotti, Gabriella, Brais, Lauren, Bueno de Mesquita, H. Ba, Basso, Daniela, Berndt, Sonja I, Boutron Ruault, Marie Christine, Bijlsma, Maarten F, Brenner, Hermann, Burdette, Laurie, Campa, Daniele, Caporaso, Neil E, Capurso, Gabriele, Cavestro, Giulia Martina, Cotterchio, Michelle, Costello, Eithne, Elena, Joanne, Boggi, Ugo, Gaziano, J. Michael, Gazouli, Maria, Giovannucci, Edward L, Goggins, Michael, Gross, Myron, Haiman, Christopher A, Hassan, Manal, Helzlsouer, Kathy J, Hu, Nan, Hunter, David J, Iskierka Jazdzewska, Elzbieta, Jenab, Mazda, Kaaks, Rudolf, Key, Timothy J, Khaw, Kay Tee, Klein, Eric A, Kogevinas, Manoli, Krogh, Vittorio, Kupcinskas, Juoza, Kurtz, Robert C, Landi, Maria T, Landi, Stefano, Le Marchand, Loic, Mambrini, Andrea, Mannisto, Satu, Milne, Roger L, Neale, Rachel E, Oberg, Ann L, Panico, Salvatore, Patel, Alpa V, Peeters, Petra H. M, Peters, Ulrike, Pezzilli, Raffaele, Porta, Miquel, Purdue, Mark, Quiros, J. Ramón, Riboli, Elio, Rothman, Nathaniel, Scarpa, Aldo, Scelo, Ghislaine, Shu, Xiao Ou, Silverman, Debra T, Soucek, Pavel, Strobel, Oliver, Sund, Malin, Małecka Panas, Ewa, Taylor, Philip R, Tavano, Francesca, Travis, Ruth C, Thornquist, Mark, Tjønneland, Anne, Tobias, Geoffrey S, Trichopoulos, Dimitrio, Vashist, Yogesh, Vodicka, Pavel, Wactawski Wende, Jean, Wentzensen, Nicola, Yu, Herbert, Yu, Kai, Zeleniuch Jacquotte, Anne, Kooperberg, Charle, Risch, Harvey A, Jacobs, Eric J, Li, Donghui, Fuchs, Charle, Hoover, Robert, Hartge, Patricia, Chanock, Stephen J, Petersen, Gloria M, Stolzenberg Solomon, Rachael S, Wolpin, Brian M, Kraft, Peter, Klein, Alison P, Canzian, Federico, Amundadottir, Laufey T., Khaw, Kay-Tee [0000-0002-8802-2903], Apollo - University of Cambridge Repository, CCA -Cancer Center Amsterdam, Center of Experimental and Molecular Medicine, Radiotherapy, Zhang, M, Wang, Z, Obazee, O, Jia, J, Childs, Ej, Hoskins, J, Figlioli, G, Mocci, E, Collins, I, Chung, Cc, Hautman, C, Arslan, Aa, Beane Freeman, L, Bracci, Pm, Buring, J, Duell, Ej, Gallinger, S, Giles, Gg, Goodman, Ge, Goodman, Pj, Kamineni, A, Kolonel, Ln, Kulke, Mh, Malats, N, Olson, Sh, Sesso, Hd, Visvanathan, K, White, E, Zheng, W, Abnet, Cc, Albanes, D, Andreotti, G, Brais, L, Bueno de Mesquita, Hb, Basso, D, Berndt, Si, Boutron Ruault, Mc, Bijlsma, Mf, Brenner, H, Burdette, L, Campa, D, Caporaso, Ne, Capurso, G, Cavestro, GIULIA MARTINA, Cotterchio, M, Costello, E, Elena, J, Boggi, U, Gaziano, Jm, Gazouli, M, Giovannucci, El, Goggins, M, Gross, M, Haiman, Ca, Hassan, M, Helzlsouer, Kj, Hu, N, Hunter, Dj, Iskierka Jazdzewska, E, Jenab, M, Kaaks, R, Key, Tj, Khaw, Kt, Klein, Ea, Kogevinas, M, Krogh, V, Kupcinskas, J, Kurtz, Rc, Landi, Mt, Landi, S, Le Marchand, L, Mambrini, A, Mannisto, S, Milne, Rl, Neale, Re, Oberg, Al, Panico, S, Patel, Av, Peeters, Ph, Peters, U, Pezzilli, R, Porta, M, Purdue, M, Quiros, Jr, Riboli, E, Rothman, N, Scarpa, A, Scelo, G, Shu, Xo, Silverman, Dt, Soucek, P, Strobel, O, Sund, M, Małecka Panas, E, Taylor, Pr, Tavano, F, Travis, Rc, Thornquist, M, Tjønneland, A, Tobias, G, Trichopoulos, D, Vashist, Y, Vodicka, P, Wactawski Wende, J, Wentzensen, N, Yu, H, Yu, K, Zeleniuch Jacquotte, A, Kooperberg, C, Risch, Ha, Jacobs, Ej, Li, D, Fuchs, C, Hoover, R, Hartge, P, Chanock, Sj, Petersen, Gm, Stolzenberg Solomon, R, Wolpin, Bm, Kraft, P, Klein, Ap, Canzian, F, and Amundadottir, L. T.
Subjects: 0301 basic medicine, Candidate gene, Pancreatic disease, GENETIC SUSCEPTIBILITY, pancreatic cancer, Datasets as Topic, Genome-wide association study, imputation, TRET, 0302 clinical medicine, Fine-mapping, GWAS, Imputation, NR5A2, Pancreatic cancer, Oncology, Genotype, Genetics, 3. Good health, fine-mapping, Chromosomes, Human, Pair 1, 030220 oncology & carcinogenesis, Chromosomes, Human, Pair 5, Chromosomes, Human, Pair 8, 616.37-006.6 [udc], BLADDER-CANCER, Single-nucleotide polymorphism, GENOTYPE IMPUTATION, BREAST, Polymorphism, Single Nucleotide, 03 medical and health sciences, Journal Article, medicine, Humans, Genetic Predisposition to Disease, GENOME-WIDE ASSOCIATION, Pàncrees -- Càncer, Cancer och onkologi, LONG-RANGE INTERACTION, business.industry, medicine.disease, Pancreatic neoplasms, genetics, Polymorphism, single nucleotide, RISK LOCI, Fold change, COMMON VARIANT, Cromosomes, Pancreatic Neoplasms, 030104 developmental biology, Cancer and Oncology, business, Imputation (genetics), LRH-1, Priority Research Paper, Genome-Wide Association Study
Abstract: Altres ajuts: The authors acknowledge the contribution of the staff of the Cancer Genomics Research Laboratory (CGR) at the National Cancer Institute, NIH, for their help throughout the project. This work was supported by the Intramural Research Program of the US National Institutes of Health (NIH), National Cancer Institute. The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the U.S. Government. Additional acknowledgements for individual participating studies are listed in the Supplemental Materials. Genome-wide association studies (GWAS) have identified common pancreatic cancer susceptibility variants at 13 chromosomal loci in individuals of European descent. To identify new susceptibility variants, we performed imputation based on 1000 Genomes (1000G) Project data and association analysis using 5,107 case and 8,845 control subjects from 27 cohort and case-control studies that participated in the PanScan I-III GWAS. This analysis, in combination with a two-staged replication in an additional 6,076 case and 7,555 control subjects from the PANcreatic Disease ReseArch (PANDoRA) and Pancreatic Cancer Case-Control (PanC4) Consortia uncovered 3 new pancreatic cancer risk signals marked by single nucleotide polymorphisms (SNPs) rs2816938 at chromosome 1q32.1 (per allele odds ratio (OR) = 1.20, P = 4.88×10 −15), rs10094872 at 8q24.21 (OR = 1.15, P = 3.22×10 −9) and rs35226131 at 5p15.33 (OR = 0.71, P = 1.70×10 −8). These SNPs represent independent risk variants at previously identified pancreatic cancer risk loci on chr1q32.1 (NR5A2), chr8q24.21 (MYC) and chr5p15.33 (CLPTM1L - TERT) as per analyses conditioned on previously reported susceptibility variants. We assessed expression of candidate genes at the three risk loci in histologically normal (n = 10) and tumor (n = 8) derived pancreatic tissue samples and observed a marked reduction of NR5A2 expression (chr1q32.1) in the tumors (fold change -7.6, P = 5.7×10 −8). This finding was validated in a second set of paired (n = 20) histologically normal and tumor derived pancreatic tissue samples (average fold change for three NR5A2 isoforms -31.3 to -95.7, P = 7.5×10 −4 -2.0×10 −3). Our study has identified new susceptibility variants independently conferring pancreatic cancer risk that merit functional follow-up to identify target genes and explain the underlying biology.
Published: 2016

19. Polygenic and multifactorial scores for pancreatic ductal adenocarcinoma risk prediction.

Author: Galeotti AA, Gentiluomo M, Rizzato C, Obazee O, Neoptolemos JP, Pasquali C, Nentwich M, Cavestro GM, Pezzilli R, Greenhalf W, Holleczek B, Schroeder C, Schöttker B, Ivanauskas A, Ginocchi L, Key TJ, Hegyi P, Archibugi L, Darvasi E, Basso D, Sperti C, Bijlsma MF, Palmieri O, Hlavac V, Talar-Wojnarowska R, Mohelnikova-Duchonova B, Hackert T, Vashist Y, Strouhal O, van Laarhoven H, Tavano F, Lovecek M, Dervenis C, Izbéki F, Padoan A, Małecka-Panas E, Maiello E, Vanella G, Capurso G, Izbicki JR, Theodoropoulos GE, Jamroziak K, Katzke V, Kaaks R, Mambrini A, Papanikolaou IS, Szmola R, Szentesi A, Kupcinskas J, Bursi S, Costello E, Boggi U, Milanetto AC, Landi S, Gazouli M, Vodickova L, Soucek P, Gioffreda D, Gemignani F, Brenner H, Strobel O, Büchler M, Vodicka P, Paiella S, Canzian F, and Campa D
Subjects: ABO Blood-Group System genetics, Alleles, Carcinoma, Pancreatic Ductal diagnosis, Carcinoma, Pancreatic Ductal genetics, Early Detection of Cancer, Female, Gene Frequency, Humans, Male, Pancreatic Neoplasms genetics, Polymorphism, Single Nucleotide, Risk Assessment, Multifactorial Inheritance
Abstract: Background: Most cases of pancreatic ductal adenocarcinoma (PDAC) are asymptomatic in early stages, and the disease is typically diagnosed in advanced phases, resulting in very high mortality. Tools to identify individuals at high risk of developing PDAC would be useful to improve chances of early detection., Objective: We generated a polygenic risk score (PRS) for PDAC risk prediction, combining the effect of known risk SNPs, and carried out an exploratory analysis of a multifactorial score., Methods: We tested the associations of the individual known risk SNPs on up to 2851 PDAC cases and 4810 controls of European origin from the PANcreatic Disease ReseArch (PANDoRA) consortium. Thirty risk SNPs were included in a PRS, which was computed on the subset of subjects that had 100% call rate, consisting of 839 cases and 2040 controls in PANDoRA and 6420 cases and 4889 controls from the previously published Pancreatic Cancer Cohort Consortium I-III and Pancreatic Cancer Case-Control Consortium genome-wide association studies. Additional exploratory multifactorial scores were constructed by complementing the genetic score with smoking and diabetes., Results: The scores were associated with increased PDAC risk and reached high statistical significance (OR=2.70, 95% CI 1.99 to 3.68, p=2.54×10 -10 highest vs lowest quintile of the weighted PRS, and OR=14.37, 95% CI 5.57 to 37.09, p=3.64×10 -8 , highest vs lowest quintile of the weighted multifactorial score)., Conclusion: We found a highly significant association between a PRS and PDAC risk, which explains more than individual SNPs and is a step forward in the direction of the construction of a tool for risk stratification in the population., Competing Interests: Competing interests: MFB has received research funding from Celgene. HvL has acted as a consultant for Celgene, and Eli Lilly and Company, Nordic Pharma Group and Philips, and has received research grants from Amgen, Bayer Schering Pharma, Celgene, Eli Lilly and Company, GlaxoSmithKline Pharmaceuticals, MSD, Nordic Pharma Group, Philips and Roche Pharmaceuticals., (© Author(s) (or their employer(s)) 2021. No commercial re-use. See rights and permissions. Published by BMJ.)
Published: 2021
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20. Mendelian randomisation study of the effects of known and putative risk factors on pancreatic cancer.

Author: Lu Y, Gentiluomo M, Lorenzo-Bermejo J, Morelli L, Obazee O, Campa D, and Canzian F
Subjects: Adenocarcinoma pathology, Adult, Aged, Body Mass Index, Carcinoma, Pancreatic Ductal complications, Carcinoma, Pancreatic Ductal pathology, Diabetes Mellitus, Type 2 complications, Diabetes Mellitus, Type 2 pathology, Female, Genome-Wide Association Study, Helicobacter Infections complications, Helicobacter Infections genetics, Helicobacter Infections pathology, Humans, Insulin genetics, Male, Mendelian Randomization Analysis, Middle Aged, Obesity complications, Obesity genetics, Obesity pathology, Polymorphism, Single Nucleotide genetics, Risk Factors, Adenocarcinoma genetics, Carcinoma, Pancreatic Ductal genetics, Diabetes Mellitus, Type 2 genetics, Genetic Predisposition to Disease
Abstract: Background: Observational studies have reported multiple risk factors for pancreatic ductal adenocarcinoma (PDAC). Some are well established, like tobacco smoking, alcohol drinking, obesity and type 2 diabetes, whereas some others are putative, such as allergy and dietary factors. Identifying causal risk factors can help establishing those that can be targeted to contribute to prevent PDAC., Objective: We sought to investigate the possible causal effects of established and putative factors on PDAC risk., Methods: We conducted a two-sample Mendelian randomisation (MR) study using publicly available data for genetic variants associated with the factors of interest, and summary genetic data from genome-wide association studies of the Pancreatic Cancer Cohort Consortium (PanScan) and the Pancreatic Cancer Case-Control Consortium (PanC4), including in total 8769 cases and 7055 controls. Causality was assessed using inverse-variance weighted, MR-Egger regression and weighted median methods, complemented with sensitivity and radial MR analyses., Results: We found evidence for a causal effect of body mass index (BMI) on PDAC risk (OR 1.43, 95% CI 1.20 to 1.71, p=8.43×10 -5 ). Fasting insulin (OR 2.84, 95% CI 1.23 to 6.56, p=0.01), low-density lipoprotein cholesterol (OR 1.16, 95% CI 1.02 to 1.32, p=0.03) and type 2 diabetes (OR 1.09, 95% CI 1.01 to 1.17, p=0.02) were also causally associated with PDAC risk. BMI showed both direct and fasting insulin-mediated causal effects., Conclusion: We found strong evidence that BMI is causally associated with PDAC risk, providing support that obesity management may be a potential prevention strategy for reducing pancreatic cancer risk while fasting insulin and type 2 diabetes showed a suggestive association that should be further investigated., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2020. No commercial re-use. See rights and permissions. Published by BMJ.)
Published: 2020
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21. Genetic polymorphisms in the cag pathogenicity island of Helicobacter pylori and risk of stomach cancer and high-grade premalignant gastric lesions.

Author: Canzian F, Rizzato C, Obazee O, Stein A, Flores-Luna L, Camorlinga-Ponce M, Mendez-Tenorio A, Vivas J, Trujillo E, Jang H, Chen W, Kasamatsu E, Bravo MM, Torres J, Muñoz N, and Kato I
Subjects: Adult, Antigens, Bacterial genetics, Bacterial Proteins genetics, Biopsy, Colombia epidemiology, DNA, Bacterial genetics, DNA, Bacterial isolation & purification, Female, Gastric Mucosa microbiology, Gastritis microbiology, Gastritis pathology, Genetic Markers, Genome, Bacterial genetics, Genomic Islands, Helicobacter Infections pathology, Helicobacter pylori isolation & purification, Helicobacter pylori pathogenicity, Humans, Male, Metaplasia microbiology, Metaplasia pathology, Mexico epidemiology, Middle Aged, Polymorphism, Genetic, Precancerous Conditions pathology, Risk Assessment methods, Risk Factors, Stomach Neoplasms microbiology, Stomach Neoplasms pathology, Whole Genome Sequencing, Gastric Mucosa pathology, Helicobacter Infections microbiology, Helicobacter pylori genetics, Precancerous Conditions microbiology, Stomach Neoplasms epidemiology
Abstract: Helicobacter pylori (Hp) infects the stomach of about half of the human population and is strongly associated with the risk of gastric cancer (GC) and its premalignant precursors. The cag pathogenicity island (cagPAI) is a region of the Hp genome encoding for key molecular machinery involved in the infection process. Following a sequencing study, we selected 50 genetic polymorphisms located in seven cagPAI genes and tested their associations with the risk of advanced gastric premalignant lesions and GC in 1220 subjects from various Latin American populations showing the whole spectrum of phenotypes from gastritis to GC. We found that three polymorphisms of cagA are associated with the risk of advanced gastric premalignant lesions (incomplete intestinal metaplasia [ie, Type 2 and 3] or dysplasia), and that six polymorphisms located in cagA, cagL and cagI were associated with risk of GC. When corrected for multiple testing none of the associations were statistically significant. However, scores built by integrating the individual polymorphisms were significantly associated with the risk of advanced gastric premalignant lesions and GC. These results have the potential of establishing markers for risk stratification in the general population, in view of targeting Hp eradication to high-risk population groups., (© 2020 The Authors. International Journal of Cancer published by John Wiley & Sons Ltd on behalf of UICC.)
Published: 2020
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22. Genome-wide association study identifies an early onset pancreatic cancer risk locus.

Author: Campa D, Gentiluomo M, Obazee O, Ballerini A, Vodickova L, Hegyi P, Soucek P, Brenner H, Milanetto AC, Landi S, Gao X, Bozzato D, Capurso G, Tavano F, Vashist Y, Hackert T, Bambi F, Bursi S, Oliverius M, Gioffreda D, Schöttker B, Ivanauskas A, Mohelnikova-Duchonova B, Darvasi E, Pezzilli R, Małecka-Panas E, Strobel O, Gazouli M, Katzke V, Szentesi A, Cavestro GM, Farkas G Jr, Izbicki JR, Moz S, Archibugi L, Hlavac V, Vincze Á, Talar-Wojnarowska R, Rusev B, Kupcinskas J, Greenhalf B, Dijk F, Giese N, Boggi U, Andriulli A, Busch OR, Vanella G, Vodicka P, Nentwich M, Lawlor RT, Theodoropoulos GE, Jamroziak K, Zuppardo RA, Moletta L, Ginocchi L, Kaaks R, Neoptolemos JP, Lucchesi M, and Canzian F
Subjects: Carcinoma, Pancreatic Ductal genetics, Carcinoma, Pancreatic Ductal pathology, Case-Control Studies, Female, Genome-Wide Association Study methods, Humans, Male, Middle Aged, Pancreas pathology, Pancreatic Neoplasms pathology, Polymorphism, Single Nucleotide genetics, Risk Factors, Pancreatic Neoplasms, Genetic Predisposition to Disease genetics, Pancreatic Neoplasms genetics
Abstract: Early onset pancreatic cancer (EOPC) is a rare disease with a very high mortality rate. Almost nothing is known on the genetic susceptibility of EOPC, therefore, we performed a genome-wide association study (GWAS) to identify novel genetic variants specific for patients diagnosed with pancreatic ductal adenocarcinoma (PDAC) at younger ages. In the first phase, conducted on 821 cases with age of onset ≤60 years, of whom 198 with age of onset ≤50, and 3227 controls from PanScan I-II, we observed four SNPs (rs7155613, rs2328991, rs4891017 and rs12610094) showing an association with EOPC risk (P < 1 × 10 -4 ). We replicated these SNPs in the PANcreatic Disease ReseArch (PANDoRA) consortium and used additional in silico data from PanScan III and PanC4. Among these four variants rs2328991 was significant in an independent set of 855 cases with age of onset ≤60 years, of whom 265 with age of onset ≤50, and 4142 controls from the PANDoRA consortium while in the in silico data, we observed no statistically significant association. However, the resulting meta-analysis supported the association (P = 1.15 × 10 -4 ). In conclusion, we propose a novel variant rs2328991 to be involved in EOPC risk. Even though it was not possible to find a mechanistic link between the variant and the function, the association is supported by a solid statistical significance obtained in the largest study on EOPC genetics present so far in the literature., (© 2020 UICC.)
Published: 2020
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23. A Transcriptome-Wide Association Study Identifies Novel Candidate Susceptibility Genes for Pancreatic Cancer.

Author: Zhong J, Jermusyk A, Wu L, Hoskins JW, Collins I, Mocci E, Zhang M, Song L, Chung CC, Zhang T, Xiao W, Albanes D, Andreotti G, Arslan AA, Babic A, Bamlet WR, Beane-Freeman L, Berndt S, Borgida A, Bracci PM, Brais L, Brennan P, Bueno-de-Mesquita B, Buring J, Canzian F, Childs EJ, Cotterchio M, Du M, Duell EJ, Fuchs C, Gallinger S, Gaziano JM, Giles GG, Giovannucci E, Goggins M, Goodman GE, Goodman PJ, Haiman C, Hartge P, Hasan M, Helzlsouer KJ, Holly EA, Klein EA, Kogevinas M, Kurtz RJ, LeMarchand L, Malats N, Männistö S, Milne R, Neale RE, Ng K, Obazee O, Oberg AL, Orlow I, Patel AV, Peters U, Porta M, Rothman N, Scelo G, Sesso HD, Severi G, Sieri S, Silverman D, Sund M, Tjønneland A, Thornquist MD, Tobias GS, Trichopoulou A, Van Den Eeden SK, Visvanathan K, Wactawski-Wende J, Wentzensen N, White E, Yu H, Yuan C, Zeleniuch-Jacquotte A, Hoover R, Brown K, Kooperberg C, Risch HA, Jacobs EJ, Li D, Yu K, Shu XO, Chanock SJ, Wolpin BM, Stolzenberg-Solomon RZ, Chatterjee N, Klein AP, Smith JP, Kraft P, Shi J, Petersen GM, Zheng W, and Amundadottir LT
Subjects: Databases, Genetic, Gene Expression, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Polymorphism, Single Nucleotide, Quantitative Trait Loci, Transcriptome, Pancreatic Neoplasms genetics
Abstract: Background: Although 20 pancreatic cancer susceptibility loci have been identified through genome-wide association studies in individuals of European ancestry, much of its heritability remains unexplained and the genes responsible largely unknown., Methods: To discover novel pancreatic cancer risk loci and possible causal genes, we performed a pancreatic cancer transcriptome-wide association study in Europeans using three approaches: FUSION, MetaXcan, and Summary-MulTiXcan. We integrated genome-wide association studies summary statistics from 9040 pancreatic cancer cases and 12 496 controls, with gene expression prediction models built using transcriptome data from histologically normal pancreatic tissue samples (NCI Laboratory of Translational Genomics [n = 95] and Genotype-Tissue Expression v7 [n = 174] datasets) and data from 48 different tissues (Genotype-Tissue Expression v7, n = 74-421 samples)., Results: We identified 25 genes whose genetically predicted expression was statistically significantly associated with pancreatic cancer risk (false discovery rate < .05), including 14 candidate genes at 11 novel loci (1p36.12: CELA3B; 9q31.1: SMC2, SMC2-AS1; 10q23.31: RP11-80H5.9; 12q13.13: SMUG1; 14q32.33: BTBD6; 15q23: HEXA; 15q26.1: RCCD1; 17q12: PNMT, CDK12, PGAP3; 17q22: SUPT4H1; 18q11.22: RP11-888D10.3; and 19p13.11: PGPEP1) and 11 at six known risk loci (5p15.33: TERT, CLPTM1L, ZDHHC11B; 7p14.1: INHBA; 9q34.2: ABO; 13q12.2: PDX1; 13q22.1: KLF5; and 16q23.1: WDR59, CFDP1, BCAR1, TMEM170A). The association for 12 of these genes (CELA3B, SMC2, and PNMT at novel risk loci and TERT, CLPTM1L, INHBA, ABO, PDX1, KLF5, WDR59, CFDP1, and BCAR1 at known loci) remained statistically significant after Bonferroni correction., Conclusions: By integrating gene expression and genotype data, we identified novel pancreatic cancer risk loci and candidate functional genes that warrant further investigation., (Published by Oxford University Press 2020. This work is written by US Government employees and is in the public domain in the US.)
Published: 2020
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24. Variations in cag pathogenicity island genes of Helicobacter pylori from Latin American groups may influence neoplastic progression to gastric cancer.

Author: Rizzato C, Torres J, Obazee O, Camorlinga-Ponce M, Trujillo E, Stein A, Mendez-Tenorio A, Bravo MM, Canzian F, and Kato I
Subjects: Gastritis microbiology, Genome, Bacterial, Humans, Latin America, Metaplasia, Nucleotide Motifs genetics, Polymorphism, Genetic, Sequence Analysis, DNA, Stomach Neoplasms pathology, Disease Progression, Genetic Variation, Genomic Islands genetics, Helicobacter pylori genetics, Stomach Neoplasms genetics, Stomach Neoplasms microbiology
Abstract: Helicobacter pylori (HP) colonizes the human stomach and induces acute gastritis, peptic ulcer disease, atrophic gastritis, and gastric adenocarcinoma. Increased virulence in HP isolates derives from harboring the cag (cytotoxin-associated genes) pathogenicity island (cagPAI). We analyzed the microvariants in cagPAI genes with the hypothesis that they may play an important role in determining HP virulence. We tested DNAs from cagA positive patients HP isolates; a total of 74 patients with chronic gastritis (CG, N = 37), intestinal metaplasia (IM, N = 21) or gastric cancer (GC, N = 16) from Mexico and Colombia. We selected 520 non-synonymous variants with at least 7.5% frequency in the original sequence outputs or with a minimum of 5 isolates with minor allele. After adjustment for multiple comparisons, no variants were statistically significantly associated with IM or GC. However, 19 non-synonymous showed conventional P-values < 0.05 comparing the frequency of the alleles between the isolates from subjects with gastritis and isolates from subjects with IM or GC; 12 of these showed a significant correlation with the severity of the disease. The present study revealed that several cagPAI genes from Latin American Western HP strains contains a number of non-synonymous variants in relatively high frequencies which could influence on the clinical outcome. However, none of the associations remained statistically significant after adjustment for multiple comparison.
Published: 2020
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25. Exome sequencing identifies germline variants in DIS3 in familial multiple myeloma.

Author: Pertesi M, Vallée M, Wei X, Revuelta MV, Galia P, Demangel D, Oliver J, Foll M, Chen S, Perrial E, Garderet L, Corre J, Leleu X, Boyle EM, Decaux O, Rodon P, Kolb B, Slama B, Mineur P, Voog E, Le Bris C, Fontan J, Maigre M, Beaumont M, Azais I, Sobol H, Vignon M, Royer B, Perrot A, Fuzibet JG, Dorvaux V, Anglaret B, Cony-Makhoul P, Berthou C, Desquesnes F, Pegourie B, Leyvraz S, Mosser L, Frenkiel N, Augeul-Meunier K, Leduc I, Leyronnas C, Voillat L, Casassus P, Mathiot C, Cheron N, Paubelle E, Moreau P, Bignon YJ, Joly B, Bourquard P, Caillot D, Naman H, Rigaudeau S, Marit G, Macro M, Lambrecht I, Cliquennois M, Vincent L, Helias P, Avet-Loiseau H, Moreno V, Reis RM, Varkonyi J, Kruszewski M, Vangsted AJ, Jurczyszyn A, Zaucha JM, Sainz J, Krawczyk-Kulis M, Wątek M, Pelosini M, Iskierka-Jażdżewska E, Grząśko N, Martinez-Lopez J, Jerez A, Campa D, Buda G, Lesueur F, Dudziński M, García-Sanz R, Nagler A, Rymko M, Jamroziak K, Butrym A, Canzian F, Obazee O, Nilsson B, Klein RJ, Lipkin SM, McKay JD, and Dumontet C
Subjects: Female, Genetic Predisposition to Disease genetics, Humans, Pedigree, Exome Sequencing methods, Exome genetics, Exosome Multienzyme Ribonuclease Complex genetics, Germ-Line Mutation genetics, Multiple Myeloma genetics
Published: 2019
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26. Genetic determinants of telomere length and risk of pancreatic cancer: A PANDoRA study.

Author: Campa D, Matarazzi M, Greenhalf W, Bijlsma M, Saum KU, Pasquali C, van Laarhoven H, Szentesi A, Federici F, Vodicka P, Funel N, Pezzilli R, Bueno-de-Mesquita HB, Vodickova L, Basso D, Obazee O, Hackert T, Soucek P, Cuk K, Kaiser J, Sperti C, Lovecek M, Capurso G, Mohelnikova-Duchonova B, Khaw KT, König AK, Kupcinskas J, Kaaks R, Bambi F, Archibugi L, Mambrini A, Cavestro GM, Landi S, Hegyi P, Izbicki JR, Gioffreda D, Zambon CF, Tavano F, Talar-Wojnarowska R, Jamroziak K, Key TJ, Fave GD, Strobel O, Jonaitis L, Andriulli A, Lawlor RT, Pirozzi F, Katzke V, Valsuani C, Vashist YK, Brenner H, and Canzian F
Subjects: Aged, Case-Control Studies, Europe, Female, Genome-Wide Association Study, Humans, Lymphocytes metabolism, Male, Middle Aged, Polymorphism, Single Nucleotide, Telomerase metabolism, Carcinoma, Pancreatic Ductal genetics, Pancreatic Neoplasms genetics, Ribonucleoproteins genetics, Telomerase genetics, Telomere metabolism, Telomere Shortening genetics
Abstract: Telomere deregulation is a hallmark of cancer. Telomere length measured in lymphocytes (LTL) has been shown to be a risk marker for several cancers. For pancreatic ductal adenocarcinoma (PDAC) consensus is lacking whether risk is associated with long or short telomeres. Mendelian randomization approaches have shown that a score built from SNPs associated with LTL could be used as a robust risk marker. We explored this approach in a large scale study within the PANcreatic Disease ReseArch (PANDoRA) consortium. We analyzed 10 SNPs (ZNF676-rs409627, TERT-rs2736100, CTC1-rs3027234, DHX35-rs6028466, PXK-rs6772228, NAF1-rs7675998, ZNF208-rs8105767, OBFC1-rs9420907, ACYP2-rs11125529 and TERC-rs10936599) alone and combined in a LTL genetic score ("teloscore", which explains 2.2% of the telomere variability) in relation to PDAC risk in 2,374 cases and 4,326 controls. We identified several associations with PDAC risk, among which the strongest were with the TERT-rs2736100 SNP (OR = 1.54; 95%CI 1.35-1.76; p = 1.54 × 10 -10 ) and a novel one with the NAF1-rs7675998 SNP (OR = 0.80; 95%CI 0.73-0.88; p = 1.87 × 10 -6 , p trend = 3.27 × 10 -7 ). The association of short LTL, measured by the teloscore, with PDAC risk reached genome-wide significance (p = 2.98 × 10 -9 for highest vs. lowest quintile; p = 1.82 × 10 -10 as a continuous variable). In conclusion, we present a novel genome-wide candidate SNP for PDAC risk (TERT-rs2736100), a completely new signal (NAF1-rs7675998) approaching genome-wide significance and we report a strong association between the teloscore and risk of pancreatic cancer, suggesting that telomeres are a potential risk factor for pancreatic cancer., (© 2018 UICC.)
Published: 2019
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27. Common genetic variants associated with pancreatic adenocarcinoma may also modify risk of pancreatic neuroendocrine neoplasms.

Author: Obazee O, Capurso G, Tavano F, Archibugi L, De Bonis A, Greenhalf W, Key T, Pasquali C, Milanetto AC, Hackert T, Fogar P, Lico V, Dervenis C, Lawlor RT, Landoni L, Gazouli M, Zambon CF, Funel N, Strobel O, Jamroziak K, Cantu C, Malecka-Panas E, Landi S, Neoptolemos JP, Basso D, Talar-Wojnarowska R, Rinzivillo M, Andriulli A, Canzian F, and Campa D
Published: 2018
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28. Genome-wide meta-analysis identifies five new susceptibility loci for pancreatic cancer.

Author: Klein AP, Wolpin BM, Risch HA, Stolzenberg-Solomon RZ, Mocci E, Zhang M, Canzian F, Childs EJ, Hoskins JW, Jermusyk A, Zhong J, Chen F, Albanes D, Andreotti G, Arslan AA, Babic A, Bamlet WR, Beane-Freeman L, Berndt SI, Blackford A, Borges M, Borgida A, Bracci PM, Brais L, Brennan P, Brenner H, Bueno-de-Mesquita B, Buring J, Campa D, Capurso G, Cavestro GM, Chaffee KG, Chung CC, Cleary S, Cotterchio M, Dijk F, Duell EJ, Foretova L, Fuchs C, Funel N, Gallinger S, M Gaziano JM, Gazouli M, Giles GG, Giovannucci E, Goggins M, Goodman GE, Goodman PJ, Hackert T, Haiman C, Hartge P, Hasan M, Hegyi P, Helzlsouer KJ, Herman J, Holcatova I, Holly EA, Hoover R, Hung RJ, Jacobs EJ, Jamroziak K, Janout V, Kaaks R, Khaw KT, Klein EA, Kogevinas M, Kooperberg C, Kulke MH, Kupcinskas J, Kurtz RJ, Laheru D, Landi S, Lawlor RT, Lee IM, LeMarchand L, Lu L, Malats N, Mambrini A, Mannisto S, Milne RL, Mohelníková-Duchoňová B, Neale RE, Neoptolemos JP, Oberg AL, Olson SH, Orlow I, Pasquali C, Patel AV, Peters U, Pezzilli R, Porta M, Real FX, Rothman N, Scelo G, Sesso HD, Severi G, Shu XO, Silverman D, Smith JP, Soucek P, Sund M, Talar-Wojnarowska R, Tavano F, Thornquist MD, Tobias GS, Van Den Eeden SK, Vashist Y, Visvanathan K, Vodicka P, Wactawski-Wende J, Wang Z, Wentzensen N, White E, Yu H, Yu K, Zeleniuch-Jacquotte A, Zheng W, Kraft P, Li D, Chanock S, Obazee O, Petersen GM, and Amundadottir LT
Subjects: Databases, Genetic, Genetic Predisposition to Disease, Genome-Wide Association Study, Hepatocyte Nuclear Factor 1-beta genetics, Hepatocyte Nuclear Factor 4 genetics, Humans, Intercellular Signaling Peptides and Proteins, Intracellular Signaling Peptides and Proteins, Polymorphism, Single Nucleotide, Proteins genetics, Repressor Proteins genetics, Tensins genetics, Carcinoma, Pancreatic Ductal genetics, Pancreatic Neoplasms genetics
Abstract: In 2020, 146,063 deaths due to pancreatic cancer are estimated to occur in Europe and the United States combined. To identify common susceptibility alleles, we performed the largest pancreatic cancer GWAS to date, including 9040 patients and 12,496 controls of European ancestry from the Pancreatic Cancer Cohort Consortium (PanScan) and the Pancreatic Cancer Case-Control Consortium (PanC4). Here, we find significant evidence of a novel association at rs78417682 (7p12/TNS3, P = 4.35 × 10 -8 ). Replication of 10 promising signals in up to 2737 patients and 4752 controls from the PANcreatic Disease ReseArch (PANDoRA) consortium yields new genome-wide significant loci: rs13303010 at 1p36.33 (NOC2L, P = 8.36 × 10 -14 ), rs2941471 at 8q21.11 (HNF4G, P = 6.60 × 10 -10 ), rs4795218 at 17q12 (HNF1B, P = 1.32 × 10 -8 ), and rs1517037 at 18q21.32 (GRP, P = 3.28 × 10 -8 ). rs78417682 is not statistically significantly associated with pancreatic cancer in PANDoRA. Expression quantitative trait locus analysis in three independent pancreatic data sets provides molecular support of NOC2L as a pancreatic cancer susceptibility gene.
Published: 2018
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29. Lack of Association for Reported Endocrine Pancreatic Cancer Risk Loci in the PANDoRA Consortium.

Author: Campa D, Obazee O, Pastore M, Panzuto F, Liço V, Greenhalf W, Katzke V, Tavano F, Costello E, Corbo V, Talar-Wojnarowska R, Strobel O, Zambon CF, Neoptolemos JP, Zerboni G, Kaaks R, Key TJ, Lombardo C, Jamroziak K, Gioffreda D, Hackert T, Khaw KT, Landi S, Milanetto AC, Landoni L, Lawlor RT, Bambi F, Pirozzi F, Basso D, Pasquali C, Capurso G, and Canzian F
Subjects: Aged, Genetic Predisposition to Disease, Humans, Middle Aged, Pancreatic Neoplasms pathology, Risk Factors, Pancreatic Neoplasms genetics
Abstract: Background: Pancreatic neuroendocrine tumors (PNETs) are rare neoplasms for which very little is known about either environmental or genetic risk factors. Only a handful of association studies have been performed so far, suggesting a small number of risk loci. Methods: To replicate the best findings, we have selected 16 SNPs suggested in previous studies to be relevant in PNET etiogenesis. We genotyped the selected SNPs (rs16944, rs1052536, rs1059293, rs1136410, rs1143634, rs2069762, rs2236302, rs2387632, rs3212961, rs3734299, rs3803258, rs4962081, rs7234941, rs7243091, rs12957119, and rs1800629) in 344 PNET sporadic cases and 2,721 controls in the context of the PANcreatic Disease ReseArch (PANDoRA) consortium. Results: After correction for multiple testing, we did not observe any statistically significant association between the SNPs and PNET risk. We also used three online bioinformatic tools (HaploReg, RegulomeDB, and GTEx) to predict a possible functional role of the SNPs, but we did not observe any clear indication. Conclusions: None of the selected SNPs were convincingly associated with PNET risk in the PANDoRA consortium. Impact: We can exclude a major role of the selected polymorphisms in PNET etiology, and this highlights the need for replication of epidemiologic findings in independent populations, especially in rare diseases such as PNETs. Cancer Epidemiol Biomarkers Prev; 26(8); 1349-51. ©2017 AACR ., (©2017 American Association for Cancer Research.)
Published: 2017
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30. Three new pancreatic cancer susceptibility signals identified on chromosomes 1q32.1, 5p15.33 and 8q24.21.

Author: Zhang M, Wang Z, Obazee O, Jia J, Childs EJ, Hoskins J, Figlioli G, Mocci E, Collins I, Chung CC, Hautman C, Arslan AA, Beane-Freeman L, Bracci PM, Buring J, Duell EJ, Gallinger S, Giles GG, Goodman GE, Goodman PJ, Kamineni A, Kolonel LN, Kulke MH, Malats N, Olson SH, Sesso HD, Visvanathan K, White E, Zheng W, Abnet CC, Albanes D, Andreotti G, Brais L, Bueno-de-Mesquita HB, Basso D, Berndt SI, Boutron-Ruault MC, Bijlsma MF, Brenner H, Burdette L, Campa D, Caporaso NE, Capurso G, Cavestro GM, Cotterchio M, Costello E, Elena J, Boggi U, Gaziano JM, Gazouli M, Giovannucci EL, Goggins M, Gross M, Haiman CA, Hassan M, Helzlsouer KJ, Hu N, Hunter DJ, Iskierka-Jazdzewska E, Jenab M, Kaaks R, Key TJ, Khaw KT, Klein EA, Kogevinas M, Krogh V, Kupcinskas J, Kurtz RC, Landi MT, Landi S, Le Marchand L, Mambrini A, Mannisto S, Milne RL, Neale RE, Oberg AL, Panico S, Patel AV, Peeters PH, Peters U, Pezzilli R, Porta M, Purdue M, Quiros JR, Riboli E, Rothman N, Scarpa A, Scelo G, Shu XO, Silverman DT, Soucek P, Strobel O, Sund M, Małecka-Panas E, Taylor PR, Tavano F, Travis RC, Thornquist M, Tjønneland A, Tobias GS, Trichopoulos D, Vashist Y, Vodicka P, Wactawski-Wende J, Wentzensen N, Yu H, Yu K, Zeleniuch-Jacquotte A, Kooperberg C, Risch HA, Jacobs EJ, Li D, Fuchs C, Hoover R, Hartge P, Chanock SJ, Petersen GM, Stolzenberg-Solomon RS, Wolpin BM, Kraft P, Klein AP, Canzian F, and Amundadottir LT
Subjects: Datasets as Topic, Genome-Wide Association Study methods, Genotype, Humans, Polymorphism, Single Nucleotide genetics, Chromosomes, Human, Pair 1 genetics, Chromosomes, Human, Pair 5 genetics, Chromosomes, Human, Pair 8 genetics, Genetic Predisposition to Disease genetics, Pancreatic Neoplasms genetics
Abstract: Genome-wide association studies (GWAS) have identified common pancreatic cancer susceptibility variants at 13 chromosomal loci in individuals of European descent. To identify new susceptibility variants, we performed imputation based on 1000 Genomes (1000G) Project data and association analysis using 5,107 case and 8,845 control subjects from 27 cohort and case-control studies that participated in the PanScan I-III GWAS. This analysis, in combination with a two-staged replication in an additional 6,076 case and 7,555 control subjects from the PANcreatic Disease ReseArch (PANDoRA) and Pancreatic Cancer Case-Control (PanC4) Consortia uncovered 3 new pancreatic cancer risk signals marked by single nucleotide polymorphisms (SNPs) rs2816938 at chromosome 1q32.1 (per allele odds ratio (OR) = 1.20, P = 4.88x10 -15), rs10094872 at 8q24.21 (OR = 1.15, P = 3.22x10 -9) and rs35226131 at 5p15.33 (OR = 0.71, P = 1.70x10 -8). These SNPs represent independent risk variants at previously identified pancreatic cancer risk loci on chr1q32.1 ( NR5A2), chr8q24.21 ( MYC) and chr5p15.33 ( CLPTM1L- TERT) as per analyses conditioned on previously reported susceptibility variants. We assessed expression of candidate genes at the three risk loci in histologically normal ( n = 10) and tumor ( n = 8) derived pancreatic tissue samples and observed a marked reduction of NR5A2 expression (chr1q32.1) in the tumors (fold change -7.6, P = 5.7x10 -8). This finding was validated in a second set of paired ( n = 20) histologically normal and tumor derived pancreatic tissue samples (average fold change for three NR5A2 isoforms -31.3 to -95.7, P = 7.5x10 -4-2.0x10 -3). Our study has identified new susceptibility variants independently conferring pancreatic cancer risk that merit functional follow-up to identify target genes and explain the underlying biology.
Published: 2016
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31. The UGT1A6_19_GG genotype is a breast cancer risk factor.

Author: Justenhoven C, Obazee O, Winter S, Rabstein S, Lotz A, Harth V, Pesch B, Brüning T, Baisch C, Hartikainen JM, Mannermaa A, Kosma VM, Kataja V, Winqvist R, Pylkäs K, Jukkola-Vuorinen A, Grip M, Fasching PA, Beckmann M, Ekici AB, Hein A, Hall P, Li J, Chang-Claude J, Flesch-Janys D, Seibold P, Rudolph A, Hamann U, Ko YD, and Brauch H
Abstract: Validation of an association between the UGT1A6_19_T>G (rs6759892) polymorphism and overall breast cancer risk. A pilot study included two population-based case-control studies from Germany (MARIE-GENICA). An independent validation study comprised four independent breast cancer case-control studies from Finland (KBCP, OBCS), Germany (BBCC), and Sweden (SASBAC). The pooled analysis included 7418 cases and 8720 controls from all six studies. Participants were of European descent. Genotyping was done by MALDI-TOF MS and statistical analysis was performed by logistic regression adjusted for age and study. The increased overall breast cancer risk for women with the UGT1A6_19_GG genotype which was observed in the pilot study was confirmed in the set of four independent study collections (OR 1.13, 95% CI 1.05-1.22; p = 0.001). The pooled study showed a similar effect (OR 1.09, 95% CI 1.04-1.14; p = 0.001). The risk effect on the basis of allele frequencies was highly significant, the pooled analysis showed an OR of 1.11 (95% CI 1.06-1.16; p = 5.8 × 10(-6)). We confirmed the association of UGT1A6_19_GG with increased overall breast cancer risk and conclude that our result from a well powered multi-stage study adds a novel candidate to the panel of validated breast cancer susceptibility loci.
Published: 2013
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32. Confirmation of the reduction of hormone replacement therapy-related breast cancer risk for carriers of the HSD17B1_937_G variant.

Author: Obazee O, Justenhoven C, Winter S, Chang-Claude J, Rudolph A, Seibold P, Flesch-Janys D, Hannelius U, Li J, Humphreys K, Hall P, Giles G, Severi G, Baglietto L, Southey M, Rabstein S, Harth V, Lotz A, Pesch B, Brüning T, Baisch C, Ko YD, Hamann U, and Brauch H
Subjects: Breast Neoplasms chemically induced, Case-Control Studies, Female, Gene Frequency, Genetic Predisposition to Disease, Heterozygote, Humans, Postmenopause, Risk Factors, Breast Neoplasms genetics, Estradiol Dehydrogenases genetics, Estrogen Replacement Therapy adverse effects, Polymorphism, Single Nucleotide
Abstract: 17β-hydroxysteroid dehydrogenase type 1 (HSD17B1) plays an important role in the biosynthesis of 17β-estradiol. The current study aimed at confirming the reduced risk of breast cancer in carriers of the non-synonymous HSD17B1_937_A>G (rs605059) polymorphism who used any hormone replacement therapy (HRT) for 10 years or longer. We performed an independent association study using four breast cancer case-control studies from Australia, Germany, and Sweden. In all, 5,777 cases and 8,189 age-matched controls of European descent were genotyped by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) and TaqMan. Risk estimates were calculated by interaction analysis and main effect analysis adjusted for age and study. Main effect analyses for women using any HRT for 10 years or longer (1,428 cases versus 1,724 controls) revealed a protective effect of the HSD17B1_937_G allele on breast cancer risk (OR 0.86, 95 % CI: 0.73-0.99; p = 0.048). Thus, our previous finding of a protective effect of the HSD17B1_937_G allele on HRT-associated breast cancer risk has now been confirmed both in independent large patient cohorts and a comprehensive pooled analysis supporting the hypothesis that a HSD17B1-mediated decreased conversion of estrone to the more potent 17β-estradiol may reduce the estrogenic effects, thereby reducing the risk of developing breast cancer during long-term HRT use.
Published: 2013
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33. The pharmacogenomics of sex hormone metabolism: breast cancer risk in menopausal hormone therapy.

Author: Justenhoven C, Obazee O, and Brauch H
Subjects: Breast Neoplasms chemically induced, Breast Neoplasms genetics, Female, Humans, Neoplasms, Hormone-Dependent genetics, Polymorphism, Genetic, Precision Medicine, Risk Factors, Treatment Outcome, Breast Neoplasms therapy, Estrogen Replacement Therapy adverse effects, Gonadal Steroid Hormones metabolism, Gonadal Steroid Hormones therapeutic use, Neoplasms, Hormone-Dependent therapy
Abstract: With women in western countries spending nearly one-third of their lifetime beyond menopause and a substantial number of these women facing severe menopausal symptoms, the goal of sex hormone pharmacogenomics is to promote the safe use of hormone replacement therapy (HRT). This could be achieved by providing molecular predictors for the upfront stratification of women in need of relief from menopausal symptoms into those with a likely benefit from HRT and those with a contraindication due to an HRT-associated breast cancer risk or other adverse effects. An increasing knowledge base of sex hormone metabolism and its variability, HRT outcomes and breast cancer susceptibility, as well as emerging examples of pharmacogenomic predictors, underscore the potential relevance of genetic variations for HRT outcome. The genes responsible for the metabolism, signaling and action of sex hormones are at the heart of this research; however, pharmacogenomic investigation of their therapeutic effects due to the enormous complexity of the biological pathways involved is still in its infancy. This article discusses the current knowledge, challenges and potential future directions towards the goal of genotype-guided safer HRT use.
Published: 2012
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34. The postmenopausal hormone replacement therapy-related breast cancer risk is decreased in women carrying the CYP2C19*17 variant.

Author: Justenhoven C, Obazee O, Winter S, Couch FJ, Olson JE, Hall P, Hannelius U, Li J, Humphreys K, Severi G, Giles G, Southey M, Baglietto L, Fasching PA, Beckmann MW, Ekici AB, Hamann U, Baisch C, Harth V, Rabstein S, Lotz A, Pesch B, Brüning T, Ko YD, and Brauch H
Subjects: Breast Neoplasms pathology, Cytochrome P-450 CYP2C19, Female, Humans, Postmenopause, Risk, Aryl Hydrocarbon Hydroxylases genetics, Breast Neoplasms genetics, Estrogen Replacement Therapy, Gonadal Steroid Hormones blood
Published: 2012
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34 results on '"Obazee, O."'

1. Antimicrobial Activities of Chloroform Extract of Whole Plant of Sida acuta Burm. f against Selected Clinical Isolates from Laboratory Samples of a Private Hospital in Benin City, Edo State, Nigeria

2. Genetic determinants of telomere length and risk of pancreatic cancer: A PANDoRA study

3. Genome-wide association study identifies an early onset pancreatic cancer risk locus

4. Germline BRCA2 K3326X and CHEK2 I157T mutations increase risk for sporadic pancreatic ductal adenocarcinoma

5. Germline BRCA2 K3326X and CHEK2 I157T mutations increase risk for sporadic pancreatic ductal adenocarcinoma

6. A multifactorial score for pancreatic ductal adenocarcinoma risk prediction

7. Genome-wide association study identifies an early onset pancreatic cancer risk locus

8. Genetic variability of the ABCC2 gene and overall survival in pancreatic cancer

9. Corrigendum: Common genetic variants associated with pancreatic adenocarcinoma may also modify risk of pancreatic neuroendocrine neoplasms [Carcinogenesis, 39, 3, (2018), (360-367)] DOI: 10.1093/carcin/bgx150

10. Genome-wide meta-analysis identifies five new susceptibility loci for pancreatic cancer

11. Common genetic variants associated with pancreatic adenocarcinoma may also modify risk of pancreatic neuroendocrine neoplasms

12. Germline BRCA2 K3326X and CHEK2 I157T mutations increase risk for sporadic pancreatic ductal adenocarcinoma

13. Genetic determinants of telomere length and risk of pancreatic cancer: a PANDoRA study

14. Do pancreatic adenocarcinoma and neuroendocrine neoplasms share genetic susceptability a PANDoRA study

15. Three new pancreatic cancer susceptibility signals identified on chromosomes 1q32.1, 5p15.33 and 8q24.21

16. Polygenic and multifactorial scores for pancreatic ductal adenocarcinoma risk prediction

17. Genome-wide association study identifies an early onset pancreatic cancer risk locus

18. Three new pancreatic cancer susceptibility signals identified on chromosomes 1q32.1, 5p15.33 and 8q24.21

19. Polygenic and multifactorial scores for pancreatic ductal adenocarcinoma risk prediction.

20. Mendelian randomisation study of the effects of known and putative risk factors on pancreatic cancer.

21. Genetic polymorphisms in the cag pathogenicity island of Helicobacter pylori and risk of stomach cancer and high-grade premalignant gastric lesions.

22. Genome-wide association study identifies an early onset pancreatic cancer risk locus.

23. A Transcriptome-Wide Association Study Identifies Novel Candidate Susceptibility Genes for Pancreatic Cancer.

24. Variations in cag pathogenicity island genes of Helicobacter pylori from Latin American groups may influence neoplastic progression to gastric cancer.

25. Exome sequencing identifies germline variants in DIS3 in familial multiple myeloma.

26. Genetic determinants of telomere length and risk of pancreatic cancer: A PANDoRA study.

27. Common genetic variants associated with pancreatic adenocarcinoma may also modify risk of pancreatic neuroendocrine neoplasms.

28. Genome-wide meta-analysis identifies five new susceptibility loci for pancreatic cancer.

29. Lack of Association for Reported Endocrine Pancreatic Cancer Risk Loci in the PANDoRA Consortium.

30. Three new pancreatic cancer susceptibility signals identified on chromosomes 1q32.1, 5p15.33 and 8q24.21.

31. The UGT1A6_19_GG genotype is a breast cancer risk factor.

32. Confirmation of the reduction of hormone replacement therapy-related breast cancer risk for carriers of the HSD17B1_937_G variant.

33. The pharmacogenomics of sex hormone metabolism: breast cancer risk in menopausal hormone therapy.

34. The postmenopausal hormone replacement therapy-related breast cancer risk is decreased in women carrying the CYP2C19*17 variant.

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34 results on '"Obazee, O."'

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