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139 results on '"Mohelnikova-Duchonova, B."'

1. A pleiotropy scan to discover new susceptibility loci for pancreatic ductal adenocarcinoma

Author

Giaccherini, M, primary, Rende, M, additional, Gentiluomo, M, additional, Corradi, C, additional, Archibugi, L, additional, Ermini, S, additional, Maiello, E, additional, Morelli, L, additional, van Eijck, C H J, additional, Cavestro, G M, additional, Schneider, M, additional, Mickevicius, A, additional, Adamonis, K, additional, Basso, D, additional, Hlavac, V, additional, Gioffreda, D, additional, Talar-Wojnarowska, R, additional, Schöttker, B, additional, Lovecek, M, additional, Vanella, G, additional, Gazouli, M, additional, Uno, M, additional, Malecka-Wojciesko, E, additional, Vodicka, P, additional, Goetz, M, additional, Bijlsma, M F, additional, Petrone, M C, additional, Bazzocchi, F, additional, Kiudelis, M, additional, Szentesi, A, additional, Carrara, S, additional, Nappo, G, additional, Brenner, H, additional, Milanetto, A C, additional, Soucek, P, additional, Katzke, V, additional, Peduzzi, G, additional, Rizzato, C, additional, Pasquali, C, additional, Chen, X, additional, Capurso, G, additional, Hackert, T, additional, Bueno-de-Mesquita, B, additional, Uzunoglu, F G G, additional, Hegyi, P, additional, Greenhalf, W, additional, Theodoropoulos, G E E, additional, Sperti, C, additional, Perri, F, additional, Oliverius, M, additional, Mambrini, A, additional, Tavano, F, additional, Farinella, R, additional, Arcidiacono, P G, additional, Lucchesi, M, additional, Bunduc, S, additional, Kupcinskas, J, additional, Di Franco, G, additional, Stocker, S, additional, Neoptolemos, J P, additional, Bambi, F, additional, Jamroziak, K, additional, Testoni, S G G, additional, Aoki, M N, additional, Mohelnikova-Duchonova, B, additional, Izbicki, J R, additional, Pezzilli, R, additional, Lawlor, R T, additional, Kauffmann, E F, additional, López de Maturana, E, additional, Malats, N, additional, Canzian, F, additional, and Campa, D, additional

Published
2024
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2. Genetic analysis of subsequent second primary malignant neoplasms in long-term pancreatic cancer survivors suggests new potential hereditary genetic alterations

Author

Lovecek M, Janatova M, Skalicky P, Zemanek T, Havlik R, Ehrmann J, Strouhal O, Zemankova P, Lhotova K, Borecka M, Soukupova J, Svebisova H, Soucek P, Hlavac V, Kleibl Z, Neoral C, Melichar B, and Mohelnikova-Duchonova B

Subjects
pancreatic ductal adenocarcinoma, second primary neoplasms, subsequent malignant neoplasm, hereditary cancer genes, long-term survivors, surgical treatment, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Martin Lovecek,1,* Marketa Janatova,2,* Pavel Skalicky,1 Tomas Zemanek,3 Roman Havlik,1 Jiri Ehrmann,4 Ondrej Strouhal,3 Petra Zemankova,2 Klara Lhotova,2 Marianna Borecka,2 Jana Soukupova,2 Hana Svebisova,3 Pavel Soucek,5 Viktor Hlavac,5 Zdenek Kleibl,2 Cestmir Neoral,1 Bohuslav Melichar,3 Beatrice Mohelnikova-Duchonova3 1Department of Surgery I, Faculty of Medicine and Dentistry, Palacky University Olomouc, University Hospital Olomouc, Olomouc, Czech Republic; 2Institute of Biochemistry and Experimental Oncology, First Faculty of Medicine, Charles University, Prague, Czech Republic; 3Department of Oncology, Institute of Molecular and Translational Medicine, Faculty of Medicine and Dentistry, Palacky University, Olomouc, Czech Republic; 4Department of Clinical and Molecular Pathology, Faculty of Medicine and Dentistry, Palacky University Olomouc, University Hospital Olomouc, Olomouc, Czech Republic; 5Biomedical Center, Faculty of Medicine in Pilsen, Charles University, Pilsen Czech Republic *These authors contributed equally to this work Background: The principal aim of this report was to study second primary malignant neoplasms (SMNs) in long-term survivors of pancreatic ductal adenocarcinoma (PDAC) with regard to the germline genetic background.Patients and methods: A total of 118 PDAC patients after a curative-intent surgery who were treated between 2006 and 2011 were analyzed. Of the 22 patients surviving for >5 years, six went on to develop SMNs. A genetic analysis of 219 hereditary cancer-predisposition and candidate genes was performed by targeted next-generation sequencing in germline DNA from 20 of these patients.Results: Of all the radically resected PDAC patients, six patients went on to subsequently develop SMNs, which accounted for 27% of the long-term survivors. The median time to diagnosis of SMNs, which included two cases of rectal cancer, and one case each of prostate cancer, malignant melanoma, breast cancer, and urinary bladder cancer, was 52.5 months. At the time of analysis, none of these patients had died as a result of PDAC progression. We identified four carriers of germline pathogenic mutations in 20 analyzed long-term survivors. One carrier of the CHEK2 mutation was found among four analyzed patients who developed SMNs. Of the remaining 16 long-term PDAC survivors, 3 patients (19%) carried germline mutation(s) in the MLH1+ ATM, CHEK2, and RAD51D gene, respectively.Conclusion: This retrospective analysis indicates that SMNs in PDAC survivors are an important clinical problem and may be more common than has been acknowledged to be the case. In patients with good performance status, surgical therapy should be considered, as the SMNs often have a favorable prognosis. Keywords: pancreatic ductal adenocarcinoma, second primary neoplasms, subsequent malignant neoplasm, hereditary cancer genes, long-term survivors, surgical treatment

Published
2019

6. Polymorphisms in Transcription Factor Binding Sites and Enhancers as Pancreatic Ductal Adenocarcinoma Risk Factors

Author

Unal, Pelin, primary, Lu, Y., additional, Aoki, M., additional, Chammas, R., additional, Gazouli, M., additional, Theodoropoulos, G., additional, van Eijck, C., additional, Bijlsma, M., additional, Dijk, F., additional, Bueno-de-Mesquita, B., additional, Kupcinskas, J., additional, Kiudelis, V., additional, Kreivenaite, E., additional, Kondrackiene, J., additional, Malecka-Wojciesko, E., additional, Talar-Wojnarowska, R., additional, Kapszewicz, M., additional, Hegyi, P., additional, Szentesi, A., additional, Eross, B., additional, Bunduc, S., additional, Mohelnikova-Duchonova, B., additional, Soucek, P., additional, Hlavac, V., additional, Oliverius, M., additional, Vodickova, L., additional, Cervena, K., additional, Hackert, T., additional, Neoptolemos, J., additional, Goetz, M., additional, Uzunoglu, F., additional, Izbicki, J., additional, Stocker, H., additional, Schöttker, B., additional, Brenner, H., additional, Perri, F., additional, Tavano, F., additional, Palmieri, O., additional, Bazzocchi, F., additional, Maiello, E., additional, Testoni, S., additional, Petrone, M., additional, Arcidiacono, P., additional, Landi, S., additional, Ermini, S., additional, Bambi, F., additional, Boggi, U., additional, Capurso, G., additional, Archibugi, L., additional, Vanella, G., additional, Cavestro, G., additional, Morelli, L., additional, Di Franco, G., additional, Milanetto, A., additional, Sperti, C., additional, Pasquali, C., additional, Basso, D., additional, Pezzilli, R., additional, Lawlor, R., additional, Capretti, G., additional, Carrara, S., additional, Campa, D., additional, and Canzian, F., additional

Published
2022
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7. Exploring the Neandertal legacy of pancreatic ductal adenocarcinoma risk in Eurasians

Author

Gentiluomo, M. Piccardi M., Bertoncini, S., Costello, E., Morelli, L., Landi, S., Milanetto, A. C., Schöttker, B., Di Franco, G., Ermini, S., Scarpa, A., Izbicki, J., Pezzilli, R., Uzunoglu, F., Talar-Wojnarowska, R., Goetz, M., Lawlor, R., Aoki, M., Bueno-de-Mesquita, B., Busch, O., Chammas, R., Tavano, F., van Laarhoven, H., Cavestro, G., Stocker, H., Bazzocchi, F., Pasquali, C., Chen, X., Puzzono, M., Ponz de Leon Pisani, R., Brenner, H., Vodickova, L., Sperti, C., Lovecek, L., Erőss, B., Basso, D., Kupcinskas, J., Vanagas, T., Janciauskas, D., Poskiene, L., Tacelli, M., Mohelnikova Duchonova, B., Capurso, G., Perri, F., Latiano, A., Mambrini, A., Maiello, E., Hegyi, P., Szentesi, A., Bunduc, S., Hussein, T., Arcidiacono, P., Boggi, U., Hackert, T., Archibugi, L., Soucek, P., Vanella, G., Lucchesi, M., Ginocchi, L., Gazouli, M., Zerbi, A., Roth, S., Jamroziak, K., Carrara, S., Hlavac, V., Oliverius, M., Neoptolemos, J., Theodoropoulos, G., van Eijck, C., Dannemann, M., Canzian, F., Tofanelli, S., and Campa, D.

Published
2022

8. Polymorphisms in transcription factor binding sites and enhancers as pancreatic ductal adenocarcinoma risk factors

Author

Unal, P., Lu, Y., Aoki, M., Chammas, R., Gazouli, M., Theodoropoulos, G., van Eijck, C., Bijlsma, M., Dijk, F., Bueno-de-Mesquita, B., Kupcinskas, J., Kiudelis, V., Kreivenaite, E., Kondrackiene, J., Malecka-Wojciesko, E., Talar-Wojnarowska, R., Kapszewicz, M., Hegyi, P., Szentesi, A., Eross, B., Bunduc, S., Mohelnikova-Duchonova, B., Soucek, P., Hlavac, V., Oliverius, M., Vodickova, L., Cervena, K., Hackert, T., Neoptolemos, J., Goetz, M., Uzunoglu, F., Izbicki, J., Stocker, H., Schöttker, B., Brenner, H., Perri, F., Tavano, F., Palmieri, O., Bazzocchi, F., Maiello, E., Testoni, S., Petrone, M., Arcidiacono, P., Landi, S., Ermini, S., Bambi, F., Boggi, U., Capurso, G., Archibugi, L., Vanella, G., Cavestro, G., Morelli, L., Di Franco, G., Milanetto, A. C., Sperti, C., Pasquali, C., Basso, D., Pezzilli, R., Lawlor, R., Capretti, G., Carrara, S., Campa, D., and Canzian, F.

Subjects
Hepatology, Endocrinology, Diabetes and Metabolism, Gastroenterology
Published
2022

9. Association of genetic variants affecting microRNAs and pancreatic cancer risk

Author

Lu, Y., Corradi, C., Gentiluomo, M., Theodoropoulos, G.E., Roth, S., Maiello, E., Morelli, L., L.Archibugi, Izbicki, J.R., Sarlós, P., Kiudelis, V., Oliverius, M., López de Maturana, E., Aoki, M.N., Vashist, Y., van Eijck, C.H.J., Gazouli, M., Talar-Wojnarowska, R., Mambrini, A., Pezzilli, R., Bueno-de-Mesquita, B., Hegyi, P., Souček, P., Neoptolemos, J., Di Franco, G., Sperti, C., Kauffmann, E.F., Hlaváč, V., Uzunoğlu, F.G., Ermini, S., Małecka-Panas, E., Lucchesi, M., Vanella, G., Dijk, F., Mohelníková-Duchoňová, B., Bambi, F., Petrone, M.C., Jamroziak, K., Guo, F., Kolarova, K., Capretti, G., Milanetto, A.C., Ginocchi, L., Loveček, M., Puzzono, M., van Laarhoven, H.W.M., Carrara, S., Ivanauskas, A., Papiris, K., Basso, D., Arcidiacono, P.G., Izbéki, F., Chammas, R., Vodicka, P., Hackert, T., Pasquali, C., Piredda, M.L., Costello-Goldring, E., Cavestro, G.M., Szentesi, A., Tavano, F., Włodarczyk, B., Brenner, H., Kreivenaite, E., Gao, X., Bunduc, S., Schneider, M.A., Latiano, A., Gioffreda, D., Testoni, S.G.G., Malats, N., Kupcinskas, J., Lawlor, R.T., Capurso, G., Campa, D., and Canzian, F.

Published
2021
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10. Lack of association of CD44-rs353630 and CHI3L2-rs684559 with pancreatic ductal adenocarcinoma survival

Author

Corradi, C., primary, Gentiluomo, M., additional, Vanella, G., additional, Johansen, A.Z., additional, Loos, M., additional, Szentesi, A., additional, Milanetto, A.C., additional, Hegyi, P., additional, Kupcinskas, J., additional, Tavano, F., additional, Schneider, M., additional, Bozzato, D., additional, Neoptolemos, J.P., additional, Hackert, T., additional, Pezzilli, R., additional, Johansen, J.S., additional, Costello, E., additional, Mohelnikova-Duchonova, B., additional, van Eijck, C.H.J., additional, Talar-Wojnarowska, R., additional, Hansen, C. Palnæs, additional, Darvasi, E., additional, Chen, I.M., additional, Cavestro, G.M., additional, Soucek, P., additional, Piredda, L., additional, Vodicka, P., additional, Gazouli, M., additional, Arcidiacono, P.G., additional, Canzian, F., additional, Campa, D., additional, and Capurso, G., additional

Published
2021
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11. Lack of association of CD44-rs353630 and CHI3L2-rs684559 with pancreatic ductal adenocarcinoma survival

Author

Gentiluomo, M. Corradi, C. Vanella, G. Johansen, A.Z. Strobel, O. Szentesi, A. Milanetto, A.C. Hegyi, P. Kupcinskas, J. Tavano, F. Neoptolemos, J.P. Bozzato, D. Hackert, T. Pezzilli, R. Johansen, J.S. Costello, E. Mohelnikova-Duchonova, B. van Eijck, C.H.J. Talar-Wojnarowska, R. Hansen, C.P. Darvasi, E. Chen, I.M. Cavestro, G.M. Soucek, P. Piredda, L. Vodicka, P. Gazouli, M. Arcidiacono, P.G. Canzian, F. Campa, D. Capurso, G.

Abstract

Although pancreatic ductal adenocarcinoma (PDAC) survival is poor, there are differences in patients’ response to the treatments. Detection of predictive biomarkers explaining these differences is of the utmost importance. In a recent study two genetic markers (CD44-rs353630 and CHI3L2-rs684559) were reported to be associated with survival after PDAC resection. We attempted to replicate the associations in 1856 PDAC patients (685 resected with stage I/II) from the PANcreatic Disease ReseArch (PANDoRA) consortium. We also analysed the combined effect of the two genotypes in order to compare our results with what was previously reported. Additional stratified analyses considering TNM stage of the disease and whether the patients received surgery were also performed. We observed no statistically significant associations, except for the heterozygous carriers of CD44-rs353630, who were associated with worse OS (HR = 5.01; 95% CI 1.58–15.88; p = 0.006) among patients with stage I disease. This association is in the opposite direction of those reported previously, suggesting that data obtained in such small subgroups are hardly replicable and should be considered cautiously. The two polymorphisms combined did not show any statistically significant association. Our results suggest that the effect of CD44-rs353630 and CHI3L2-rs684559 cannot be generalized to all PDAC patients. © 2021, The Author(s).

Published
2021

12. 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
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13. Associations between pancreatic expression quantitative trait loci (eQTLs) and pancreatic ductal adenocarcinoma risk

Author

Gentiluomo, M., Pistoni, L., Peduzzi, G., Lu, Y., Macauda, A., Hlavac, V., Vanella, G., Darvasi, E., Milanetto, A. C., Oliverius, M., Vashist, Y., Di Leo, M., Mohelnikova-Duchonova, B., Talar-Wojnarowska, R., Gheorghe, C., Petrone, M., Strobel, O., Arcidiacono, P., Vodickova, L., Szentesi, A., Capurso, G., Gajdan, L., Malleo, G., Theodoropoulos, G., Basso, D., Soucek, P., Brenner, H., Lawlor, R., Morelli, L., Ivanauskas, A., Kauffmann, E., Gazouli, M. Archibugi L., Nentwich, M., Lovecek, M., Cavestro, G., Vodicka, P., Landi, S., Tavano, F., Sperti, C., Hackert, T., Kupcinsckas, J., Pezzilli, R., Andriulli, A., Pollina, L., Kreivenaite, E., Gioffreda, D., Jamroziak, K., Hegyi, P., Izbicki, J., Testoni, S., Zuppardo, R., Bozzato, D., Neoptolemos, J., Canzian, F., and Campa, D

Published
2020

14. Polymorphic variants with non-coding RNA and risk of pancreatic ductal adenocarcinoma

Author

Gentiluomo, M., Corradi, C., Lu, Y., Giaccherini, M., Hegyi, P., Pezzilli, R., Tavano, F., Szentesi, A., Gajdan, L., Nentwich, M., Strobel, O., Gazouli, M., Cavestro, G., Darvasi, E., Arcidiacono, P., Landi, S., Luchini, C., Gioffreda, D., Kupcinsckas, J., Hackert, T., Neoptolemos, J., Morelli, L., Kreivenaite, E., Zuppardo, R., Carrara, S., Di Franco, G., Brenner, H., Hlavac, V., Sperti, C., Milanetto, A. C., Moz, S., Mohelnikova-Duchonova, B., Petrone, M., Lawlor, R., Vanella, G., Vashist, Y., Soucek, P., Vodicka, P., Cervena, K., Capurso, G., Malenka-Panas, E., Pasquali, C., Archibugi, L., Gheorghe, C., Andriulli, A., Ivanauskas, A., Theodoropoulos, G., Jamroziak, K., Izbicki, J., Testoni, S., Oliverius, M., Napoli, N., Canzian, F., and Campa, D.

Published
2020

15. 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

19. 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

20. 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

21. 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

22. 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

23. 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, 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, and 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 <0.05 considered significant. K3326X and I157T were associated with increased risk of developing sporadic PDAC (odds ratio (ORdom ) = 1.78, 95% confidence interval (CI) = 1.26-2.52, p = 1.19 × 10-3 and ORdom = 1.74, 95% CI = 1.15-2.63, p = 8.57 × 10-3 , respectively). Neither mutation was significantly associated with risk of developing early-onset PDAC. This retrospective study demonstrates novel risk estimates of K3326X and I157T in sporadic PDAC which suggest that upon validation and in combination with other established genetic and non-genetic risk factors, these mutations may be used to improve pancreatic cancer risk assessment in European populations. Identification of carriers of these risk alleles as high-risk groups may also facilitate screening or prevention strategies for such individuals, regardless of family history.

Published
2019

24. SLC22A3 polymorphisms may influence overall patient survival-PANDORA study

Author

Mohelnikova-Duchonova, B, Strouhal, O, Hughes, Dj, Lovecek, M, Holcatova, I, Oliverius, M, Kala, Z, Campa, D, Rizzato, C, Canzian, F, Pezzilli, R, Talar-Wojnarowska, R, Malecka-Panas, E, Sperti, C, Zambon, Cf, Pedrazzoli, S, Fogar, P, Milanetto, A. C., Capurso, G, Delle Fave, G, Valente, R, Gazouli, M, Malleo, G, Lawlor, Rt, Strobel, O, Hackert, T, Giese, N, Vodicka, P, Vodickova, L, Landi, S, Tavano, F, Gioffreda, D, Piepoli, A, Pazienza, V, Mambrini, A, Bursi, S, Pacetti, P, Bambi, F, Ermini, S, Funel, N, and Soucek, P

Published
2018

25. Do pancreatic cancer and chronic pancreatitis share the same genetic risk factors? A PANcreatic Disease ReseArch (PANDoRA) consortium investigation

Author

Campa, D. Pastore, M. Capurso, G. Hackert, T. Di Leo, M. Izbicki, J.R. Khaw, K.-T. Gioffreda, D. Kupcinskas, J. Pasquali, C. Macinga, P. Kaaks, R. Stigliano, S. Peeters, P.H. Key, T.J. Talar-Wojnarowska, R. Vodicka, P. Valente, R. Vashist, Y.K. Salvia, R. Papaconstantinou, I. Shimizu, Y. Valsuani, C. Zambon, C.F. Gazouli, M. Valantiene, I. Niesen, W. Mohelnikova-Duchonova, B. Hara, K. Soucek, P. Malecka-Panas, E. Bueno-de-Mesquita, H.B. Johnson, T. Brenner, H. Tavano, F. Fogar, P. Ito, H. Sperti, C. Butterbach, K. Latiano, A. Andriulli, A. Cavestro, G.M. Busch, O.R.C. Dijk, F. Greenhalf, W. Matsuo, K. Lombardo, C. Strobel, O. König, A.-K. Cuk, K. Strothmann, H. Katzke, V. Cantore, M. Mambrini, A. Oliverius, M. Pezzilli, R. Landi, S. Canzian, F.

Subjects
endocrine system diseases, digestive system diseases
Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a very aggressive tumor with a five-year survival of less than 6%. Chronic pancreatitis (CP), an inflammatory process in of the pancreas, is a strong risk factor for PDAC. Several genetic polymorphisms have been discovered as susceptibility loci for both CP and PDAC. Since CP and PDAC share a consistent number of epidemiologic risk factors, the aim of this study was to investigate whether specific CP risk loci also contribute to PDAC susceptibility. We selected five common SNPs (rs11988997, rs379742, rs10273639, rs2995271 and rs12688220) that were identified as susceptibility markers for CP and analyzed them in 2,914 PDAC cases, 356 CP cases and 5,596 controls retrospectively collected in the context of the international PANDoRA consortium. We found a weak association between the minor allele of the PRSS1-PRSS2-rs10273639 and an increased risk of developing PDAC (ORhomozygous = 1.19, 95% CI 1.02–1.38, p = 0.023). Additionally all the SNPs confirmed statistically significant associations with risk of developing CP, the strongest being PRSS1-PRSS2-rs10273639 (ORheterozygous = 0.51, 95% CI 0.39–0.67, p = 1.10 × 10−6) and MORC4-rs 12837024 (ORhomozygous = 2.07 (1.55–2.77, ptrend = 0.7 × 10−11). Taken together, the results from our study do not support variants rs11988997, rs379742, rs10273639, rs2995271 and rs12688220 as strong predictors of PDAC risk, but further support the role of these SNPs in CP susceptibility. Our study suggests that CP and PDAC probably do not share genetic susceptibility, at least in terms of high frequency variants. © 2017 UICC

Published
2018

29. 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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30. 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, Gaziano, JMM, 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, K-T, Klein, EA, Kogevinas, M, Kooperberg, C, Kulke, MH, Kupcinskas, J, Kurtz, RJ, Laheru, D, Landi, S, Lawlor, RT, Lee, I-M, LeMarchand, L, Lu, L, Malats, N, Mambrini, A, Mannisto, S, Milne, RL, Mohelnikova-Duchonova, 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, X-O, 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, Amundadottir, LT, 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, Gaziano, JMM, 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, K-T, Klein, EA, Kogevinas, M, Kooperberg, C, Kulke, MH, Kupcinskas, J, Kurtz, RJ, Laheru, D, Landi, S, Lawlor, RT, Lee, I-M, LeMarchand, L, Lu, L, Malats, N, Mambrini, A, Mannisto, S, Milne, RL, Mohelnikova-Duchonova, 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, X-O, 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

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

31. Identification of recessively inherited genetic variants for pancreatic cancer risk

Author

Lu, Y., Gentiluomo, M., Macauda, A., Gioffreda, D., Gazouli, M., Petrone, M.C., Kelemen, D., L.Ginocchi, Morelli, L., Papiris, K., Greenhalf, W., Izbicki, J.R., Kiudelis, V., Mohelníková-Duchoňová, B., Bueno-de-Mesquita, B., Vodicka, P., Brenner, H., Diener, M.K., Pezzilli, R., Ivanauskas, A., Salvia, R., Szentesi, A., Aoki, M.N., Németh, B.C., Sperti, C., Jamroziak, K., Chammas, R., Oliverius, M., Archibugi, L., Ermini, S., Novák, J., Kupcinskas, J., Strouhal, O., Souček, P., Cavestro, G.M., Milanetto, A.C., Vanella, G., Neoptolemos, J.P., Theodoropoulos, G.E., van Laarhoven, H.W.M., Mambrini, A., Moz, S., Kala, Z., Loveček, M., Basso, D., Uzunoglu, F.G., Hackert, T., Testoni, S.G.G., Hlavac, V., Andriulli, A., Lucchesi, M., Tavano, F., Carrara, S., Hegyi, P., Arcidiacono, P.G., Busch, O.R., Lawlor, R.T., Puzzono, M., Boggi, U., Guo, F., Małecka-Panas, E., Capurso, G., Landi, S., R.Talar-Wojnarowska, Strobel, O., Gao, X., Vashist, Y., Campa, D., and Canzian, F.

Published
2021
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32. Association of variants of genes involved in mitochondrial metabolism with pancreatic cancer risk

Author

Peduzzi, G., Gentiluomo, M., Tavano, F., Arcidiacono, P.G., Ermini, S., Boggi, U., Cavestro, G.M., Capurso, G., Morelli, L., Milanetto, A.C., Pezzilli, R., Lawlor, R.T., Carrara, S., Lovecek, M., Souček, P., Vodičková, Guo, F., Hackert, T., Uzunoğlu, F.G., Gazouli, M., Párniczky, A., Kupcinskas, J., Bijlsm, M.F., Bueno-de-Mesquita, B., Vermeulen, R.C.H., van Eijck, C.H.J., Jamroziak, K., Talar-Wojnarowska, R., Greenhalf, W., Gioffreda, D., Petrone, M.C., Landi, S., Archibugi, L., Puzzono, M., Funel, N., Sperti, C., Piredda, M.L., Mohelnikova-Duchonova, B., Hlaváč, V., Gao, X., Schneider, M., Izbicki, J.R., Theodoropoulos, G., Bunduc, S., Kreivenaite, E., Busch, O.R., Małecka-Panas, E., Costello, E., Perri, F., Testoni, S.G.G., Vanella, G., Pasquali, C., Oliverius, M., H.Brenner, Loos, M., Götz, M., Georgiou, K., Erőss, B., Maiello, E., Szentes i, A., Bazzocchi, F., Basso, D., Neoptolemos, J.P., Hegyi, P., Kiudelis, V., Canzian, F., and Campa, D.

Published
2021
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33. Do pancreatic cancer and chronic pancreatitis share the same genetic risk factors? A PANcreatic Disease ReseArch (PANDoRA) consortium investigation

Author

Campa, D, Pastore, M, Capurso, G, Hackert, T, Di Leo, M, Izbicki, JR, Khaw, K-T, Gioffreda, D, Kupcinskas, J, Pasquali, C, Macinga, P, Kaaks, R, Stigliano, S, Peeters, PH, Key, TJ, Talar-Wojnarowska, R, Vodicka, P, Valente, R, Vashist, YK, Salvia, R, Papaconstantinou, I, Shimizu, Y, Valsuani, C, Zambon, CF, Gazouli, M, Valantiene, I, Niesen, W, Mohelnikova-Duchonova, B, Hara, K, Soucek, P, Malecka-Panas, E, Bueno-de-Mesquita, HBA, Johnson, T, Brenner, H, Tavano, F, Fogar, P, Ito, H, Sperti, C, Butterbach, K, Latiano, A, Andriulli, A, Cavestro, GM, Busch, ORC, Dijk, F, Greenhalf, W, Matsuo, K, Lombardo, C, Strobel, O, König, A-K, Cuk, K, Strothmann, H, Katzke, V, Cantore, M, Mambrini, A, Oliverius, M, Pezzilli, R, Landi, S, Canzian, F, Other departments, CCA - Imaging and biomarkers, AGEM - Amsterdam Gastroenterology Endocrinology Metabolism, Campa, Daniele, Pastore, Manuela, Capurso, Gabriele, Hackert, Thilo, Di Leo, Milena, Izbicki, Jakob R, Khaw, Kay tee, Gioffreda, Domenica, Kupcinskas, Juoza, Pasquali, Claudio, Macinga, Peter, Kaaks, Rudolf, Stigliano, Serena, Peeters, Petra H, Key, Timothy J, Talar wojnarowska, Renata, Vodicka, Pavel, Valente, Roberto, Vashist, Yogesh K, Salvia, Roberto, Papaconstantinou, Ioanni, Shimizu, Yasuhiro, Valsuani, Chiara, Zambon, Carlo Federico, Gazouli, Maria, Valantiene, Irena, Niesen, Willem, Mohelnikova duchonova, Beatrice, Hara, Kazuo, Soucek, Pavel, Malecka panas, Ewa, Bueno de mesquita, H. Ba, Johnson, Theron, Brenner, Herman, Tavano, Francesca, Fogar, Paola, Ito, Hidemi, Sperti, Cosimo, Butterbach, Katja, Latiano, Anna, Andriulli, Angelo, Cavestro, GIULIA MARTINA, Busch, Olivier R. C, Dijk, Frederike, Greenhalf, William, Matsuo, Keitaro, Lombardo, Carlo, Strobel, Oliver, König, Anna katharina, Cuk, Katarina, Strothmann, Hendrik, Katzke, Verena, Cantore, Maurizio, Mambrini, Andrea, Oliverius, Martin, Pezzilli, Raffaele, Landi, Stefano, and Canzian, Federico

Subjects
Adult, Male, Cancer Research, endocrine system diseases, Chronic pancreatiti, pancreatic ductal adenocarcinoma, Adenocarcinoma, Polymorphism, Single Nucleotide, genetic polymorphisms, Risk Factors, Pancreatitis, Chronic, Biomarkers, Tumor, genetic polymorphism, Humans, Trypsin, Chronic, Polymorphism, Aged, Retrospective Studies, Tumor, Carcinoma, association, Nuclear Proteins, Single Nucleotide, Middle Aged, ACUTE PANCREATITIS, Prognosis, digestive system diseases, PANCREATIC CANCER, Pancreatic Neoplasms, Pancreatitis, Oncology, Pancreatic Ductal, Case-Control Studies, Chronic pancreatitis, Carcinoma, Pancreatic Ductal, Female, Follow-Up Studies, Trypsinogen, Biomarkers
Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a very aggressive tumor with a five-year survival of less than 6%. Chronic pancreatitis (CP), an inflammatory process in of the pancreas, is a strong risk factor for PDAC. Several genetic polymorphisms have been discovered as susceptibility loci for both CP and PDAC. Since CP and PDAC share consistent number of epidemiologic risk factors, the aim of this study was to investigate whether specific CP risk loci also contribute to PDAC susceptibility. We selected five common SNPs (rs11988997, rs379742, rs10273639 rs2995271 and rs12688220) that were identified as susceptibility markers for CP and analyzed them in 2,914 PDAC cases, 356 CP cases and 5,596 controls retrospectively collected in the context of the international PANDoRA consortium. We found a weak association between the minor allele of the PRSS1-PRSS2-rs10273639 and an increased risk of developing PDAC (ORhomozygous =1.19, 95% CI 1.02-1.38, p=0.023). Additionally all the SNPs confirmed statistically significant associations with risk of developing CP, the strongest being PRSS1-PRSS2-rs10273639 (ORheterozygous =0.51, 95% CI 0.39-0.67, p=1.10x10(-6) ) and MORC4-rs 12837024 (ORhomozygous =2.07 (1.55-2.77, ptrend =0.7x10(-11) ). Taken together, the results from our study do not support variants rs11988997, rs379742, rs10273639 rs2995271 and rs12688220 as strong predictors of PDAC risk, but further support the role of these SNPs in CP susceptibility. Our study suggests that CP and PDAC probably do not share genetic susceptibility, at least in terms of high frequency variants. This article is protected by copyright. All rights reserved.

Published
2017

34. SLC22A3 polymorphisms do not modify pancreatic cancer risk, but may influence overall patient survival

Author

Mohelnikova-Duchonova, B. Strouhal, O. Hughes, D.J. Holcatova, I. Oliverius, M. Kala, Z. Campa, D. Rizzato, C. Canzian, F. Pezzilli, R. Talar-Wojnarowska, R. Malecka-Panas, E. Sperti, C. Federico Zambon, C. Pedrazzoli, S. Fogar, P. Milanetto, A.C. Capurso, G. Delle Fave, G. Valente, R. Gazouli, M. Malleo, G. Teresa Lawlor, R. Strobel, O. Hackert, T. Giese, N. Vodicka, P. Vodickova, L. Landi, S. Tavano, F. Gioffreda, D. Piepoli, A. Pazienza, V. Mambrini, A. Pedata, M. Cantore, M. Bambi, F. Ermini, S. Funel, N. Lemstrova, R. Soucek, P.

Abstract

Expression of the solute carrier (SLC) transporter SLC22A3 gene is associated with overall survival of pancreatic cancer patients. This study tested whether genetic variability in SLC22A3 associates with pancreatic cancer risk and prognosis. Twenty four single nucleotide polymorphisms (SNPs) tagging the SLC22A3 gene sequence and regulatory elements were selected for analysis. Of these, 22 were successfully evaluated in the discovery phase while six significant or suggestive variants entered the validation phase, comprising a total study number of 1,518 cases and 3,908 controls. In the discovery phase, rs2504938, rs9364554, and rs2457571 SNPs were significantly associated with pancreatic cancer risk. Moreover, rs7758229 associated with the presence of distant metastases, while rs512077 and rs2504956 correlated with overall survival of patients. Although replicated, the association for rs9364554 did not pass multiple testing corrections in the validation phase. Contrary to the discovery stage, rs2504938 associated with survival in the validation cohort, which was more pronounced in stage IV patients. In conclusion, common variation in the SLC22A3 gene is unlikely to significantly contribute to pancreatic cancer risk. The rs2504938 SNP in SLC22A3 significantly associates with an unfavorable prognosis of pancreatic cancer patients. Further investigation of this SNP effect on the molecular and clinical phenotype is warranted. © 2017 The Author(s).

Published
2017

37. Functional single nucleotide polymorphisms within the cyclindependent kinase inhibitor 2A/2B region affect pancreatic cancer risk

Author

Campa, D. Pastore, M. Gentiluomo, M. Talar-Wojnarowska, R. Kupcinskas, J. Malecka-Panas, E. Neoptolemos, J.P. Niesen, W. Vodicka, P. Delle Fave, G. Bas Bueno-de-Mesquita, H. Gazouli, M. Pacetti, P. Di Leo, M. Ito, H. Klüter, H. Soucek, P. Corbo, V. Yamao, K. Hosono, S. Kaaks, R. Vashist, Y. Gioffreda, D. Strobel, O. Shimizu, Y. Dijk, F. Andriulli, A. Ivanauskas, A. Bugert, P. Tavano, F. Vodickova, L. Zambon, C.F. Lovecek, M. Landi, S. Key, T.J. Boggi, U. Pezzilli, R. Jamroziak, K. Mohelnikova-Duchonova, B. Mambrini, A. Bambi, F. Busch, O. Pazienza, V. Valente, R. Theodoropoulos, G.E. Hackert, T. Capurso, G. Cavestro, G.M. Pasquali, C. Basso, D. Sperti, C. Matsuo, K. Büchler, M. Khaw, K.-T. Izbicki, J. Costello, E. Katzke, V. Michalski, C. Stepien, A. Rizzato, C. Canzian, F.

Abstract

The CDKN2A (p16) gene plays a key role in pancreatic cancer etiology. It is one of the most commonly somatically mutated genes in pancreatic cancer, rare germline mutations have been found to be associated with increased risk of developing familiar pancreatic cancer and CDKN2A promoter hyper-methylation has been suggested to play a critical role both in pancreatic cancer onset and prognosis. In addition several unrelated SNPs in the 9p21.3 region, that includes the CDNK2A, CDNK2B and the CDNK2B-AS1 genes, are associated with the development of cancer in various organs. However, association between the common genetic variability in this region and pancreatic cancer risk is not clearly understood. We sought to fill this gap in a case-control study genotyping 13 single nucleotide polymorphisms (SNPs) in 2,857 pancreatic ductal adenocarcinoma (PDAC) patients and 6,111 controls in the context of the Pancreatic Disease Research (PANDoRA) consortium. We found that the A allele of the rs3217992 SNP was associated with an increased pancreatic cancer risk (ORhet=1.14, 95% CI 1.01-1.27, p=0.026, ORhom=1.30, 95% CI 1.12-1.51, p=0.00049). This pleiotropic variant is reported to be a mir-SNP that, by changing the binding site of one or more miRNAs, could influence the normal cell cycle progression and in turn increase PDAC risk. In conclusion, we observed a novel association in a pleiotropic region that has been found to be of key relevance in the susceptibility to various types of cancer and diabetes suggesting that the CDKN2A/B locus could represent a genetic link between diabetes and pancreatic cancer risk.

Published
2016

38. Polymorphism of taste receptor genes (TASRs) and risk of pancreatic cancer

Author

Campa, D., Gentiluomo, M., Rizzato, C., Neoptolemos, J. P., Talar Wojnarowska, R., Costello, E., Mohelnikova Duchonova, B., Strobel, O., Malecka Panas, E., Jamroziak, K., Khaw, K. T., Capurso, G., Lemstrova, R., Vodicka, P., Zambon, CARLO-FEDERICO, Giese, N., Basso, Daniela, Theodoropoulos, G. E., Tavano, F., Vodichova, L., Sperti, Cosimo, Dalle Fave, G., Pezzilli, R., Archibugi, L., Hackert, T., Mambrini, A., Mafficini, A., Gazouli, M., Landi, S., Bugert, P., Souceck, P., De Bonis, A., Maiello, E., Pasquali, Claudio, Pacetti, P., Key, T. J., Bambi, F., Kluter, H., Cantore, M., Funel, N., Barale, R., and Canzian, F.

Published
2016

39. Novel pancreatic cancer susceptibility loci discovered through genome-wild association studies

Author

Canzian, F., Campa, D., Rizzato, C., Bijlsma, M. F., Brenner, H., Bueno de Mesquita, H. B., Capurso, G., Cavestro, G. M., Funel, N., Gazouli, M., Hackert, T., Key, T. J., Kupcinskas, J., Landi, S., Małecka Panas, E., Mambrini, A., Mohelnikova Duchonova, B., Neoptolemos, J. P., Pasquali, Claudio, Pezzilli, R., Scarpa, A., Strobel, O., Tavano, F., Vahist, Y. K., Vodicka, P., Stolzenberg Solomon, R., Wolpin, B., Klein, A., and Amundadottir, L. T.

Published
2015

40. Common variation at 2p13.3, 3q29, 7p13 and 17q25.1 associated with susceptibility to pancreatic cancer

Author

Childs, E.J. Mocci, E. Campa, D. Bracci, P.M. Gallinger, S. Goggins, M. Li, D. Neale, R.E. Olson, S.H. Scelo, G. Amundadottir, L.T. Bamlet, W.R. Bijlsma, M.F. Blackford, A. Borges, M. Brennan, P. Brenner, H. Bueno-De-Mesquita, H.B. Canzian, F. Capurso, G. Cavestro, G.M. Chaffee, K.G. Chanock, S.J. Cleary, S.P. Cotterchio, M. Foretova, L. Fuchs, C. Funel, N. Gazouli, M. Hassan, M. Herman, J.M. Holcatova, I. Holly, E.A. Hoover, R.N. Hung, R.J. Janout, V. Key, T.J. Kupcinskas, J. Kurtz, R.C. Landi, S. Lu, L. Malecka-Panas, E. Mambrini, A. Mohelnikova-Duchonova, B. Neoptolemos, J.P. Oberg, A.L. Orlow, I. Pasquali, C. Pezzilli, R. Rizzato, C. Saldia, A. Scarpa, A. Stolzenberg-Solomon, R.Z. Strobel, O. Tavano, F. Vashist, Y.K. Vodicka, P. Wolpin, B.M. Yu, H. Petersen, G.M. Risch, H.A. Klein, A.P.

Abstract

Pancreatic cancer is the fourth leading cause of cancer death in the developed world. Both inherited high-penetrance mutations in BRCA2 (ref. 2), ATM, PALB2 (ref. 4), BRCA1 (ref. 5), STK11 (ref. 6), CDKN2A and mismatch-repair genes and low-penetrance loci are associated with increased risk. To identify new risk loci, we performed a genome-wide association study on 9,925 pancreatic cancer cases and 11,569 controls, including 4,164 newly genotyped cases and 3,792 controls in 9 studies from North America, Central Europe and Australia. We identified three newly associated regions: 17q25.1 (LINC00673, rs11655237, odds ratio (OR) = 1.26, 95% confidence interval (CI) = 1.19-1.34, P = 1.42 × 10-14), 7p13 (SUGCT, rs17688601, OR = 0.88, 95% CI = 0.84-0.92, P = 1.41 × 10-8) and 3q29 (TP63, rs9854771, OR = 0.89, 95% CI = 0.85-0.93, P = 2.35 × 10-8). We detected significant association at 2p13.3 (ETAA1, rs1486134, OR = 1.14, 95% CI = 1.09-1.19, P = 3.36 × 10-9), a region with previous suggestive evidence in Han Chinese. We replicated previously reported associations at 9q34.2 (ABO), 13q22.1 (KLF5), 5p15.33 (TERT and CLPTM1), 13q12.2 (PDX1), 1q32.1 (NR5A2), 7q32.3 (LINC-PINT), 16q23.1 (BCAR1) and 22q12.1 (ZNRF3). Our study identifies new loci associated with pancreatic cancer risk. © 2015 Nature America, Inc. All rights reserved.

Published
2015

42. TERT gene harbors multiple variants associated with pancreatic cancer susceptibility

Author

Campa, D. Rizzato, C. Stolzenberg-Solomon, R. Pacetti, P. Vodicka, P. Cleary, S.P. Capurso, G. Bueno-De-Mesquita, H.B. Werner, J. Gazouli, M. Butterbach, K. Ivanauskas, A. Giese, N. Petersen, G.M. Fogar, P. Wang, Z. Bassi, C. Ryska, M. Theodoropoulos, G.E. Kooperberg, C. Li, D. Greenhalf, W. Pasquali, C. Hackert, T. Fuchs, C.S. Mohelnikova-Duchonova, B. Sperti, C. Funel, N. Dieffenbach, A.K. Wareham, N.J. Buring, J. Holcátová, I. Costello, E. Zambon, C.-F. Kupcinskas, J. Risch, H.A. Kraft, P. Bracci, P.M. Pezzilli, R. Olson, S.H. Sesso, H.D. Hartge, P. Strobel, O. Małecka-Panas, E. Visvanathan, K. Arslan, A.A. Pedrazzoli, S. Souček, P. Gioffreda, D. Key, T.J. Talar-Wojnarowska, R. Scarpa, A. Mambrini, A. Jacobs, E.J. Jamroziak, K. Klein, A. Tavano, F. Bambi, F. Landi, S. Austin, M.A. Vodickova, L. Brenner, H. Chanock, S.J. Delle Fave, G. Piepoli, A. Cantore, M. Zheng, W. Wolpin, B.M. Amundadottir, L.T. Canzian, F.

Abstract

A small number of common susceptibility loci have been identified for pancreatic cancer, one of which is marked by rs401681 in the TERT-CLPTM1L gene region on chromosome 5p15.33. Because this region is characterized by low linkage disequilibrium, we sought to identify whether additional single nucleotide polymorphisms (SNPs) could be related to pancreatic cancer risk, independently of rs401681. We performed an in-depth analysis of genetic variability of the telomerase reverse transcriptase (TERT) and the telomerase RNA component (TERC) genes, in 5,550 subjects with pancreatic cancer and 7,585 controls from the PANcreatic Disease ReseArch (PANDoRA) and the PanScan consortia. We identified a significant association between a variant in TERT and pancreatic cancer risk (rs2853677, odds ratio=0.85; 95% confidence interval=0.80-0.90, p=8.3 × 10-8). Additional analysis adjusting rs2853677 for rs401681 indicated that the two SNPs are independently associated with pancreatic cancer risk, as suggested by the low linkage disequilibrium between them (r2=0.07, D′=0.28). Three additional SNPs in TERT reached statistical significance after correction for multiple testing: rs2736100 (p=3.0 × 10-5), rs4583925 (p=4.0 × 10-5) and rs2735948 (p=5.0 × 10-5). In conclusion, we confirmed that the TERT locus is associated with pancreatic cancer risk, possibly through several independent variants. What's new? Most pancreatic cancer patients do not survive long after diagnosis, and, so far, there are not many genetic markers to help screen for the disease. In search of genetic predictors of pancreatic cancer, the authors zoomed in on a region linked to susceptibility to the disease. They measured the frequency of different variants of two genes, telomerase reverse transcriptase and telomerase RNA component, among thousands of pancreatic cancer patients and controls. They identified several variants of the TERT gene that indicate a boosted pancreatic cancer risk, and which may develop into useful prognostic tools. © 2015 UICC.

Published
2015

43. Hedgehog pathway overexpression in pancreatic cancer is abrogated by new-generation taxoid SB-T-1216

Author

Mohelnikova-Duchonova, B, primary, Kocik, M, additional, Duchonova, B, additional, Brynychova, V, additional, Oliverius, M, additional, Hlavsa, J, additional, Honsova, E, additional, Mazanec, J, additional, Kala, Z, additional, Ojima, I, additional, Hughes, D J, additional, Doherty, J E, additional, Murray, H A, additional, Crockard, M A, additional, Lemstrova, R, additional, and Soucek, P, additional

Published
2016
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44. Lack of replication of seven pancreatic cancer susceptibility loci identified in two Asian populations

Author

Campa, D. Rizzato, C. Bauer, A.S. Werner, J. Capurso, G. Costello, E. Talar-Wojnarowska, R. Jamroziak, K. Pezzilli, R. Gazouli, M. Khaw, K.-T. Key, T.J. Bambi, F. Mohelnikova-Duchonova, B. Heller, A. Landi, S. Vodickova, L. Theodoropoulos, G. Bugert, P. Vodicka, P. Hoheisel, J.D. Delle Fave, G. Neoptolemos, J.P. Soucek, P. Büchler, M.W. Giese, N. Canzian, F.

Subjects
endocrine system diseases
Abstract

Background: Two recent genome-wide association studies (GWAS) of pancreatic ductal adenocarcinoma (PDAC), conducted, respectively, in a Japanese and in a Chinese population, identified eight novel loci affecting PDAC risk. Methods: We attempted to replicate the novel loci in a series of PDACs and healthy controls of European ancestry in the context of the newly formed PANcreatic Disease ReseArch (PANDoRA) consortium. We genotyped seven single-nucleotide polymorphisms (SNP): rs12413624, rs1547374, rs372883, rs5768709, rs6464375, rs708224, rs9502893 (one SNP identified in the Chinese GWAS is not polymorphic in Caucasians) in 1,299PDACcases and 2,884 controls.Wealso attempted stratified analysis considering the different stages of the disease and addressed the possible involvement of the selected SNPs on the survival of patients. Results: None of the SNPs were significantly associated with PDAC risk if considering the overall population of the consortium. When stratifying for country of origin, we found that in the Polish subgroup, the G allele of rs372883 was statistically significantly associated with increased risk [OR, 6.40;95% confidence interval (CI), 2.28-17.91]. However, the sample size of the subgroups was rather small; therefore, this result can be due to chance. None of the SNPs was associated with disease progression or survival. Conclusions: None of the SNPs associated with PDAC risk in two Asian populations were convincingly associated with PDAC risk in individuals of European descent. Impact: This study illustrates the importance of evaluation of PDAC risk markers across ethnic groups. © 2012 American Association for Cancer Research.

Published
2013

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