@article{MTMT:34797929,
	title = {A pleiotropy scan to discover new susceptibility loci for pancreatic ductal adenocarcinoma},
	url = {https://m2.mtmt.hu/api/publication/34797929},
	author = {Giaccherini, M and Rende, M and Gentiluomo, M and Corradi, C and Archibugi, L and Ermini, S and Maiello, E and Morelli, L and van Eijck, C H J and Cavestro, G M and Schneider, M and Mickevicius, A and Adamonis, K and Basso, D and Hlavac, V and Gioffreda, D and Talar-Wojnarowska, R and Schöttker, B and Lovecek, M and Vanella, G and Gazouli, M and Uno, M and Malecka-Wojciesko, E and Vodicka, P and Goetz, M and Bijlsma, M F and Petrone, M C and Bazzocchi, F and Kiudelis, M and Szentesi, Andrea Ildikó and Carrara, S and Nappo, G and Brenner, H and Milanetto, A C and Soucek, P and Katzke, V and Peduzzi, G and Rizzato, C and Pasquali, C and Chen, X and Capurso, G and Hackert, T and Bueno-de-Mesquita, B and Uzunoglu, F G G and Hegyi, Péter and Greenhalf, W and Theodoropoulos, G E E and Sperti, C and Perri, F and Oliverius, M and Mambrini, A and Tavano, F and Farinella, R and Arcidiacono, P G and Lucchesi, M and Bunduc, Stefania and Kupcinskas, J and Di Franco, G and Stocker, S and Neoptolemos, J P and Bambi, F and Jamroziak, K and Testoni, S G G and Aoki, M N and Mohelnikova-Duchonova, B and Izbicki, J R and Pezzilli, R and Lawlor, R T and Kauffmann, E F and López de Maturana, E and Malats, N and Canzian, F and Campa, D},
	doi = {10.1093/mutage/geae012},
	journal-iso = {MUTAGENESIS},
	journal = {MUTAGENESIS},
	unique-id = {34797929},
	issn = {0267-8357},
	abstract = {Pleiotropic variants (i.e., genetic polymorphisms influencing more than one phenotype) are often associated with cancer risk. A scan of pleiotropic variants was successfully conducted ten years ago in relation to pancreatic ductal adenocarcinoma susceptibility. However, in the last decade, genetic association studies performed on several human traits have greatly increased the number of known pleiotropic variants. Based on the hypothesis that variants already associated with a least one trait have a higher probability of association with other traits, 61,052 variants reported to be associated by at least one genome wide association study (GWAS) with at least one human trait were tested in the present study consisting of two phases (discovery and validation), comprising a total of 16,055 pancreatic ductal adenocarcinoma (PDAC) cases and 212,149 controls. The meta-analysis of the two phases showed two loci (10q21.1-rs4948550 (P=6.52×10-5) and 7q36.3-rs288762 (P=3.03×10-5) potentially associated with PDAC risk. 10q21.1-rs4948550 shows a high degree of pleiotropy and it is also associated with colorectal cancer risk while 7q36.3-rs288762 is situated 28,558 base pairs upstream of the Sonic Hedgehog (SHH) gene, which is involved in the cell differentiation process and PDAC etiopathogenesis. In conclusion, none of the single nucleotide polymorphisms (SNPs) showed a formally statistically significant association after correction for multiple testing. However, given their pleiotropic nature and association with various human traits including colorectal cancer, the two SNPs showing the best associations with PDAC risk merit further investigation through fine mapping and ad hoc functional studies.},
	keywords = {single nucleotide polymorphism; genetic susceptibility; Pancreatic cancer; Pleiotropy},
	year = {2024},
	eissn = {1464-3804},
	orcid-numbers = {Szentesi, Andrea Ildikó/0000-0003-2097-6927; Hegyi, Péter/0000-0003-0399-7259}
}

@article{MTMT:34561485,
	title = {Polymorphisms in transcription factor binding sites and enhancer regions and pancreatic ductal adenocarcinoma risk},
	url = {https://m2.mtmt.hu/api/publication/34561485},
	author = {Ünal, Pelin and Lu, Ye and Bueno-de-Mesquita, Bas and van Eijck, Casper H J and Talar-Wojnarowska, Renata and Szentesi, Andrea Ildikó and Gazouli, Maria and Kreivenaite, Edita and Tavano, Francesca and Małecka-Wojciesko, Ewa and Erőss, Bálint Mihály and Oliverius, Martin and Bunduc, Stefania and Nóbrega Aoki, Mateus and Vodickova, Ludmila and Boggi, Ugo and Giaccherini, Matteo and Kondrackiene, Jurate and Chammas, Roger and Palmieri, Orazio and Theodoropoulos, George E and Bijlsma, Maarten F and Basso, Daniela and Mohelnikova-Duchonova, Beatrice and Soucek, Pavel and Izbicki, Jakob R and Kiudelis, Vytautas and Vanella, Giuseppe and Arcidiacono, Paolo Giorgio and Włodarczyk, Barbara and Hackert, Thilo and Schöttker, Ben and Uzunoglu, Faik G and Bambi, Franco and Goetz, Mara and Hlavac, Viktor and Brenner, Hermann and Perri, Francesco and Carrara, Silvia and Landi, Stefano and Hegyi, Péter and Dijk, Frederike and Maiello, Evaristo and Capretti, Giovanni and Testoni, Sabrina Gloria Giulia and Petrone, Maria Chiara and Stocker, Hannah and Ermini, Stefano and Archibugi, Livia and Gentiluomo, Manuel and Cavestro, Giulia Martina and Pezzilli, Raffaele and Di Franco, Gregorio and Milanetto, Anna Caterina and Sperti, Cosimo and Neoptolemos, John P and Morelli, Luca and Vokacova, Klara and Pasquali, Claudio and Lawlor, Rita T and Bazzocchi, Francesca and Kupcinskas, Juozas and Capurso, Gabriele and Campa, Daniele and Canzian, Federico},
	doi = {10.1186/s40246-024-00576-x},
	journal-iso = {HUM GENOMICS},
	journal = {HUMAN GENOMICS},
	volume = {18},
	unique-id = {34561485},
	issn = {1473-9542},
	abstract = {Genome-wide association studies (GWAS) are a powerful tool for detecting variants associated with complex traits and can help risk stratification and prevention strategies against pancreatic ductal adenocarcinoma (PDAC). However, the strict significance threshold commonly used makes it likely that many true risk loci are missed. Functional annotation of GWAS polymorphisms is a proven strategy to identify additional risk loci. We aimed to investigate single-nucleotide polymorphisms (SNP) in regulatory regions [transcription factor binding sites (TFBSs) and enhancers] that could change the expression profile of multiple genes they act upon and thereby modify PDAC risk. We analyzed a total of 12,636 PDAC cases and 43,443 controls from PanScan/PanC4 and the East Asian GWAS (discovery populations), and the PANDoRA consortium (replication population). We identified four associations that reached study-wide statistical significance in the overall meta-analysis: rs2472632(A) (enhancer variant, OR 1.10, 95%CI 1.06,1.13, p = 5.5 × 10-8), rs17358295(G) (enhancer variant, OR 1.16, 95%CI 1.10,1.22, p = 6.1 × 10-7), rs2232079(T) (TFBS variant, OR 0.88, 95%CI 0.83,0.93, p = 6.4 × 10-6) and rs10025845(A) (TFBS variant, OR 1.88, 95%CI 1.50,1.12, p = 1.32 × 10-5). The SNP with the most significant association, rs2472632, is located in an enhancer predicted to target the coiled-coil domain containing 34 oncogene. Our results provide new insights into genetic risk factors for PDAC by a focused analysis of polymorphisms in regulatory regions and demonstrating the usefulness of functional prioritization to identify loci associated with PDAC risk.},
	keywords = {single nucleotide polymorphism; ENHANCER; Pancreatic cancer; Association study; Transcription factor binding site},
	year = {2024},
	eissn = {1479-7364},
	orcid-numbers = {Szentesi, Andrea Ildikó/0000-0003-2097-6927; Erőss, Bálint Mihály/0000-0003-3658-8427; Hegyi, Péter/0000-0003-0399-7259}
}

@article{MTMT:34434496,
	title = {Discharge protocol in acute pancreatitis: an international survey and cohort analysis},
	url = {https://m2.mtmt.hu/api/publication/34434496},
	author = {Nagy, Rita and Ocskay, Klementina and Sipos, Zoltán and Szentesi, Andrea Ildikó and Vincze, Áron and Czakó, László and Izbéki, Ferenc and Shirinskaya, Natalia V and Poluektov, Vladimir L and Zolotov, Alexandr N and Zhu, Yin and Xia, Liang and He, Wenhua and Sutton, Robert and Szatmary, Peter and Mukherjee, Rajarshi and Burridge, Isobel Saffron and Wauchope, Emma and Francisco, Elsa and Aparicio, David and Pinto, Bruno and Gomes, António and Nunes, Vitor and Tantau, Vasile Marcel and Sagau, Emanuela Denisa and Tantau, Alina Ioana and Suceveanu, Andra Iulia and Tocia, Cristina and Dumitru, Andrei and Pando, Elizabeth and Alberti, Piero and Cirera, Arturo and Molero, Xavier and Lee, Hong Sik and Jung, Min Kyu and Kim, Eui Joo and Lee, Sanghyub and Rebollo, María Lourdes Ruiz and Nistal, Reyes Busta and Santervas, Sandra Izquierdo and Lesko, Dusan and Soltes, Marek and Radonak, Jozef and Zatorski, Hubert and Małecka-Panas, Ewa and Fabisiak, Adam and Yaroslav, M Susak and Mykhailo, V Maksymenko and Olekcandr, A Tkachenko and Barauskas, Giedrius and Simanaitis, Vytautas and Ignatavicius, Povilas and Jinga, Mariana and Balaban, Vasile-Daniel and Patoni, Cristina and Gong, Liang and Song, Kai and Li, Yunlong and Gonçalves, T Cúrdia and Freitas, Marta and Macedo, Vítor and Vornhuelz, Marlies and Klauss, Sarah and Beyer, Georg and Koksal, Aydin Seref and Tozlu, Mukaddes and Eminler, Ahmet Tarik and Monclús, Nuria Torres and Comas, Eva Pijoan and Oballe, Juan Armando Rodriguez and Nawacki, Łukasz and Głuszek, Stanisław and Rama-Fernández, Alberto and Galego, Marco and de la Iglesia, Daniel and Aykut, Umut Emre and Duman, Deniz Güney and Aslan, Rahmi and Gherbon, Adriana and Deng, Lihui and Huang, Wei and Xia, Qing and Poropat, Goran and Radovan, Anja and Vranić, Luka and Ricci, Claudio and Ingaldi, Carlo and Casadei, Riccardo and Negoi, Ionut and Ciubotaru, Cezar and Iordache, Florin Mihail and Constantinescu, Gabriel and Sandru, Vasile and Altintas, Engin and Balci, Hatice Rizaoglu and Constantino, Júlio and Aveiro, Débora and Pereira, Jorge and Gunay, Suleyman and Misirlioglu Sucan, Seda and Dronov, Oleksiy and Kovalska, Inna and Bush, Nikhil and Rana, Surinder Singh and Chooklin, Serge and Chuklin, Serhii and Saizu, Ionut Adrian and Gheorghe, Cristian and Göltl, Philipp and Hirth, Michael and Mateescu, Radu Bogdan and Papuc, Geanina and Minkov, Georgi Angelov and Enchev, Emil Tihomirov and Mastrangelo, Laura and Jovine, Elio and Chen, Weiwei and Zhu, Quping and Gąsiorowska, Anita and Fabisiak, Natalia and Bezmarevic, Mihailo and Litvin, Andrey and Mottes, Martina Cattani and Choi, Eun Kwang and Bánovčin, Peter and Nosáková, Lenka and Kovacheva-Slavova, Mila Dimitrova and Kchaou, Ali and Tlili, Ahmed and Marino, Marco V and Kusnierz, Katarzyna and Mickevicius, Artautas and Hollenbach, Marcus and Molcan, Pavol and Ioannidis, Orestis and Tokarev, Mark Valerievich and Ince, Ali Tüzün and Semenenko, Ivan Albertovich and Galeev, Shamil and Ramírez-Maldonado, Elena and Sallinen, Ville and Pencik, Petr and Bajor, Judit and Sarlós, Patrícia and Hágendorn, Roland and Gódi, Szilárd and Szabó, Imre and Czimmer, József and Pár, Gabriella and Illés, Anita and Faluhelyi, Nándor and Kanizsai, Péter László and Nagy, Tamás and Mikó, Alexandra and Németh, Balázs and Hamvas, József and Bod, Barnabás and Varga, Márta and Török, Imola and Novák, János and Patai, Árpád and Sümegi, János and Góg, Csaba and Papp, Mária and Erőss, Bálint Mihály and Váncsa, Szilárd and Teutsch, Brigitta and Márta, Katalin and Hegyi, Péter Jenő and Tornai, Tamás and Lázár, Balázs and Hussein, Tamás and Tarján, Dorottya and Lipp, Mónika Bernadett and Kovács, Beáta and Urbán, Orsolya and Fürst, Emese Rita and Tari, Edina and Kocsis, Ibolya and Maurovich-Horvat, Pál and Tihanyi, Balázs and Eperjesi, Orsolya and Kormos, Zita and Deák, Pál Ákos and Párniczky, Andrea and Hegyi, Péter},
	doi = {10.1038/s41598-023-48480-z},
	journal-iso = {SCI REP},
	journal = {SCIENTIFIC REPORTS},
	volume = {13},
	unique-id = {34434496},
	issn = {2045-2322},
	abstract = {There are several overlapping clinical practice guidelines in acute pancreatitis (AP), however, none of them contains suggestions on patient discharge. The Hungarian Pancreatic Study Group (HPSG) has recently developed a laboratory data and symptom-based discharge protocol which needs to be validated. (1) A survey was conducted involving all members of the International Association of Pancreatology (IAP) to understand the characteristics of international discharge protocols. (2) We investigated the safety and effectiveness of the HPSG-discharge protocol. According to our international survey, 87.5% (49/56) of the centres had no discharge protocol. Patients discharged based on protocols have a significantly shorter median length of hospitalization (LOH) (7 (5;10) days vs. 8 (5;12) days) p < 0.001), and a lower rate of readmission due to recurrent AP episodes (p = 0.005). There was no difference in median discharge CRP level among the international cohorts (p = 0.586). HPSG-protocol resulted in the shortest LOH (6 (5;9) days) and highest median CRP (35.40 (13.78; 68.40) mg/l). Safety was confirmed by the low rate of readmittance (n = 35; 5%). Discharge protocol is necessary in AP. The discharge protocol used in this study is the first clinically proven protocol. Developing and testifying further protocols are needed to better standardize patients' care.},
	year = {2023},
	eissn = {2045-2322},
	orcid-numbers = {Nagy, Rita/0000-0002-2663-4912; Ocskay, Klementina/0000-0001-5848-2506; Sipos, Zoltán/0000-0001-7845-8116; Szentesi, Andrea Ildikó/0000-0003-2097-6927; Vincze, Áron/0000-0003-2217-7686; Czakó, László/0000-0002-6331-0802; Izbéki, Ferenc/0000-0001-7767-4319; Sarlós, Patrícia/0000-0002-5086-9455; Czimmer, József/0000-0001-7831-3523; Kanizsai, Péter László/0000-0001-7896-2857; Nagy, Tamás/0000-0001-5437-1411; Németh, Balázs/0000-0001-5338-7577; Papp, Mária/0000-0003-3662-4010; Erőss, Bálint Mihály/0000-0003-3658-8427; Váncsa, Szilárd/0000-0002-9347-8163; Teutsch, Brigitta/0000-0002-9530-7886; Márta, Katalin/0000-0002-2213-4865; Tari, Edina/0000-0002-8540-0614; Kocsis, Ibolya/0000-0003-3128-2832; Maurovich-Horvat, Pál/0000-0003-0885-736X; Hegyi, Péter/0000-0003-0399-7259}
}

@article{MTMT:34196830,
	title = {CFTR p.F508del Mutation Carrier Status Is Not Associated With Biliary Acute Pancreatitis},
	url = {https://m2.mtmt.hu/api/publication/34196830},
	author = {Martonosi, Ágnes Rita and Németh, Balázs Csaba and Párniczky, Andrea and Vincze, Áron and Szentesi, Andrea Ildikó and Erőss, Bálint Mihály and Sahin-Tóth, Miklós and Hegyi, Péter and Hegyi, Eszter},
	doi = {10.1097/MPA.0000000000002241},
	journal-iso = {PANCREAS},
	journal = {PANCREAS},
	volume = {52},
	unique-id = {34196830},
	issn = {0885-3177},
	year = {2023},
	eissn = {1536-4828},
	pages = {e256-e257},
	orcid-numbers = {Martonosi, Ágnes Rita/0000-0001-6528-4671; Vincze, Áron/0000-0003-2217-7686; Szentesi, Andrea Ildikó/0000-0003-2097-6927; Erőss, Bálint Mihály/0000-0003-3658-8427; Hegyi, Péter/0000-0003-0399-7259}
}

@article{MTMT:34133723,
	title = {A scan of all coding region variants of the human genome, identifies 13q12.2-rs9579139 and 15q24.1-rs2277598 as novel risk loci for pancreatic ductal adenocarcinoma},
	url = {https://m2.mtmt.hu/api/publication/34133723},
	author = {Giaccherini, Matteo and Gori, Leonardo and Gentiluomo, Manuel and Farinella, Riccardo and Cervena, Klara and Skieceviciene, Jurgita and Dijk, Frederike and Capurso, Gabriele and Vezakis, Antonis and Archibugi, Livia and Chammas, Roger and Hussein, Tamás and Tavano, Francesca and Hegyi, Péter and Lovecek, Martin and Izbicki, Jakob and Brenner, Hermann and Mohelnikova-Duchonova, Beatrice and Dell'Anna, Giuseppe and Kupcinskas, Juozas and Ermini, Stefano and Aoki, Mateus Nóbrega and Neoptolemos, John P and Gazouli, Maria and Pasquali, Claudio and Pezzilli, Raffaele and Talar-Wojnarowska, Renata and Oliverius, Martin and Al-Saeedi, Mohammed and Lucchesi, Maurizio and Furbetta, Niccolò and Carrara, Silvia and van Eijck, Casper H J and Maleckas, Almantas and Milanetto, Anna Caterina and Lawlor, Rita T and Schöttker, Ben and Boggi, Ugo and Morelli, Luca and Ginocchi, Laura and Ponz de Leon, Ruggero and Sperti, Cosimo and Zerbi, Alessandro and Arcidiacono, Paolo Giorgio and Uzunoglu, Faik G and Bunduc, Stefania and Holleczek, Bernd and Gioffreda, Domenica and Małecka-Wojciesko, Ewa and Kiudelis, Mindaugas and Szentesi, Andrea Ildikó and van Laarhoven, Hanneke W M and Soucek, Pavel and Götz, Mara and Erőss, Bálint Mihály and Cavestro, Giulia Martina and Basso, Daniela and Perri, Francesco and Landi, Stefano and Canzian, Federico and Campa, Daniele},
	doi = {10.1093/carcin/bgad056},
	journal-iso = {CARCINOGENESIS},
	journal = {CARCINOGENESIS},
	volume = {44},
	unique-id = {34133723},
	issn = {0143-3334},
	abstract = {Coding sequence variants comprise a small fraction of the germline genetic variability of the human genome. However, they often cause deleterious change in protein function and are therefore associated with pathogenic phenotypes. To identify novel pancreatic ductal adenocarcinoma (PDAC) risk loci, we carried out a complete scan of all common missense and synonymous SNPs and analysed them in a case control study comprising four different populations, for a total of 14,538 PDAC cases and 190,657 controls. We observed a statistically significant association between 13q12.2-rs9581957-T and PDAC risk (P=2.46x10 -9), that is in linkage disequilibrium (LD) with a deleterious missense variant (rs9579139) of the URAD gene. Recent findings suggest that this gene is active in peroxisomes. Considering that peroxisomes have a key role as molecular scavengers, especially in eliminating reactive oxygen species, a malfunctioning URAD protein might expose the cell to a higher load of potentially DNA damaging molecules and therefore increase PDAC risk. The association was observed in individuals of European and Asian ethnicity. We also observed the association of the missense variant 15q24.1-rs2277598-T, that belongs to BBS4 gene, with increased PDAC risk (P=1.53x10 -6). rs2277598 is associated with body mass index and is in LD with diabetes susceptibility loci. In conclusion, we identified two missense variants associated with the risk of developing PDAC independently from the ethnicity highlighting the importance of conducting reanalysis of GWAS studies in light of functional data.},
	keywords = {genetic susceptibility; SINGLE NUCLEOTIDE POLYMORPHISMS; Association study; Pancreatic ductal adenocarcinoma; missense},
	year = {2023},
	eissn = {1460-2180},
	pages = {642-649},
	orcid-numbers = {Hegyi, Péter/0000-0003-0399-7259; Szentesi, Andrea Ildikó/0000-0003-2097-6927; Erőss, Bálint Mihály/0000-0003-3658-8427}
}

@article{MTMT:34103680,
	title = {Exploring the Neandertal legacy of pancreatic ductal adenocarcinoma risk in Eurasians},
	url = {https://m2.mtmt.hu/api/publication/34103680},
	author = {Piccardi, Margherita and Gentiluomo, Manuel and Bertoncini, Stefania and Pezzilli, Raffaele and Erőss, Bálint Mihály and Bunduc, Stefania and Uzunoglu, Faik G and Talar-Wojnarowska, Renata and Vanagas, Tomas and Sperti, Cosimo and Oliverius, Martin and Aoki, Mateus Nóbrega and Ermini, Stefano and Hussein, Tamás and Boggi, Ugo and Jamroziak, Krzysztof and Maiello, Evaristo and Morelli, Luca and Vodickova, Ludmila and Di Franco, Gregorio and Landi, Stefano and Szentesi, Andrea Ildikó and Lovecek, Martin and Puzzono, Marta and Tavano, Francesca and van Laarhoven, Hanneke W M and Zerbi, Alessandro and Mohelnikova-Duchonova, Beatrice and Stocker, Hannah and Costello, Eithne and Capurso, Gabriele and Ginocchi, Laura and Lawlor, Rita T and Vanella, Giuseppe and Bazzocchi, Francesca and Izbicki, Jakob R and Latiano, Anna and Bueno-de-Mesquita, Bas and Ponz de Leon Pisani, Ruggero and Schöttker, Ben and Soucek, Pavel and Hegyi, Péter and Gazouli, Maria and Hackert, Thilo and Kupcinskas, Juozas and Poskiene, Lina and Tacelli, Matteo and Roth, Susanne and Carrara, Silvia and Perri, Francesco and Hlavac, Viktor and Theodoropoulos, George E and Busch, Olivier R and Mambrini, Andrea and van Eijck, Casper H J and Arcidiacono, Paolo and Scarpa, Aldo and Pasquali, Claudio and Basso, Daniela and Lucchesi, Maurizio and Milanetto, Anna Caterina and Neoptolemos, John P and Cavestro, Giulia Martina and Janciauskas, Dainius and Chen, Xuechen and Chammas, Roger and Goetz, Mara and Brenner, Hermann and Archibugi, Livia and Dannemann, Michael and Canzian, Federico and Tofanelli, Sergio and Campa, Daniele},
	doi = {10.1186/s40659-023-00457-y},
	journal-iso = {BIOL RES},
	journal = {BIOLOGICAL RESEARCH},
	volume = {56},
	unique-id = {34103680},
	issn = {0716-9760},
	abstract = {The genomes of present-day non-Africans are composed of 1-3% of Neandertal-derived DNA as a consequence of admixture events between Neandertals and anatomically modern humans about 50-60 thousand years ago. Neandertal-introgressed single nucleotide polymorphisms (aSNPs) have been associated with modern human disease-related traits, which are risk factors for pancreatic ductal adenocarcinoma (PDAC), such as obesity, type 2 diabetes, and inflammation. In this study, we aimed at investigating the role of aSNPs in PDAC in three Eurasian populations.The high-coverage Vindija Neandertal genome was used to select aSNPs in non-African populations from 1000 Genomes project phase 3 data. Then, the association between aSNPs and PDAC risk was tested independently in Europeans and East Asians, using existing GWAS data on more than 200 000 individuals. We did not find any significant associations between aSNPs and PDAC in samples of European descent, whereas, in East Asians, we observed that the Chr10p12.1-rs117585753-T allele (MAF = 10%) increased the risk to develop PDAC (OR = 1.35, 95%CI 1.19-1.54, P = 3.59 × 10-6), with a P-value close to a threshold that takes into account multiple testing.Our results show only a minimal contribution of Neandertal SNPs to PDAC risk.},
	keywords = {Pancreatic cancer; Association study; introgression; ADMIXTURE; Neandertal; Eurasians},
	year = {2023},
	eissn = {0717-6287},
	orcid-numbers = {Erőss, Bálint Mihály/0000-0003-3658-8427; Szentesi, Andrea Ildikó/0000-0003-2097-6927; Hegyi, Péter/0000-0003-0399-7259}
}

@article{MTMT:34072590,
	title = {Invalidity of Tokyo guidelines in acute biliary pancreatitis : A multicenter cohort analysis of 944 pancreatitis cases},
	url = {https://m2.mtmt.hu/api/publication/34072590},
	author = {Juhász, Márk Félix and Tóháti, Rebeka and Jászai, Viktória Adrienn and Molnár, Regina and Borbásné Farkas, Kornélia and Czakó, László and Vincze, Áron and Erőss, Bálint Mihály and Szentesi, Andrea Ildikó and Izbéki, Ferenc and Papp, Mária and Hegyi, Péter and Párniczky, Andrea},
	doi = {10.1002/ueg2.12402},
	journal-iso = {UEG JOURNAL},
	journal = {UNITED EUROPEAN GASTROENTEROLOGY JOURNAL},
	volume = {11},
	unique-id = {34072590},
	issn = {2050-6406},
	abstract = {There is a noteworthy overlap between the clinical picture of biliary acute pancreatitis (AP) and the 2018 Tokyo guidelines currently used for the diagnosis of cholangitis (AC) and cholecystitis (CC). This can lead to significant antibiotic and endoscopic retrograde cholangiopancreatography (ERCP) overuse.We aimed to assess the on-admission prevalence of AC/CC according to the 2018 Tokyo guidelines (TG18) in a cohort of biliary AP patients, and its association with antibiotic use, ERCP and clinically relevant endpoints.We conducted a secondary analysis of the Hungarian Pancreatic Study Group's prospective multicenter registry of 2195 AP cases. We grouped and compared biliary cases (n = 944) based on the on-admission fulfillment of definite AC/CC according to TG18. Aside from antibiotic use, we evaluated mortality, AC/CC/AP severity, ERCP performance and length of hospitalization. We also conducted a literature review discussing each criteria of the TG18 in the context of AP.27.8% of biliary AP cases fulfilled TG18 for both AC and CC, 22.5% for CC only and 20.8% for AC only. Antibiotic use was high (77.4%). About 2/3 of the AC/CC cases were mild, around 10% severe. Mortality was below 1% in mild and moderate AC/CC patients, but considerably higher in severe cases (12.8% and 21.2% in AC and CC). ERCP was performed in 89.3% of AC cases, common bile duct stones were found in 41.1%.Around 70% of biliary AP patients fulfilled the TG18 for AC/CC, associated with a high rate of antibiotic use. Mortality in presumed mild or moderate AC/CC is low. Each of the laboratory and clinical criteria are commonly fulfilled in biliary AP, single imaging findings are also unspecific-AP specific diagnostic criteria are needed, as the prevalence of AC/CC are likely greatly overestimated. Randomized trials testing antibiotic use are also warranted.},
	keywords = {MORTALITY; Antibiotic use; cholangitis; endoscopic retrograde cholangiopancreatography; cholecystitis; ERCP; STONES; Biliary acute pancreatitis; 2018 Tokyo guidelines},
	year = {2023},
	eissn = {2050-6414},
	pages = {767-774},
	orcid-numbers = {Molnár, Regina/0009-0009-7067-1647; Borbásné Farkas, Kornélia/0000-0002-5349-6527; Czakó, László/0000-0002-6331-0802; Vincze, Áron/0000-0003-2217-7686; Erőss, Bálint Mihály/0000-0003-3658-8427; Szentesi, Andrea Ildikó/0000-0003-2097-6927; Izbéki, Ferenc/0000-0001-7767-4319; Papp, Mária/0000-0003-3662-4010; Hegyi, Péter/0000-0003-0399-7259; Váncsa, Szilárd/0000-0002-9347-8163; Márta, Katalin/0000-0002-2213-4865; Nagy, Rita/0000-0002-2663-4912; Imrei, Marcell/0000-0003-0175-7462; Maurovich-Horvat, Pál/0000-0003-0885-736X; Doros, Attila/0000-0002-6496-9895; Zubek, László/0000-0003-0583-3290; Gál, János/0000-0001-9160-6478}
}

@article{MTMT:34011872,
	title = {Risk of chronic pancreatitis in carriers of the c.180C>T (p.Gly60=) CTRC variant: Case-control studies and meta-analysis},
	url = {https://m2.mtmt.hu/api/publication/34011872},
	author = {Berke, Gergő and Beer, Sebastian and Gede, Noémi and Takáts, Amanda and Szentesi, Andrea Ildikó and Hegyi, Péter and Rosendahl, Jonas and Sahin-Tóth, Miklós and Németh, Balázs and Hegyi, Eszter},
	doi = {10.1016/j.pan.2023.05.013},
	journal-iso = {PANCREATOLOGY},
	journal = {PANCREATOLOGY},
	volume = {23},
	unique-id = {34011872},
	issn = {1424-3903},
	year = {2023},
	eissn = {1424-3911},
	pages = {481-490},
	orcid-numbers = {Berke, Gergő/0000-0002-7822-2637; Szentesi, Andrea Ildikó/0000-0003-2097-6927; Hegyi, Péter/0000-0003-0399-7259; Rosendahl, Jonas/0000-0003-4513-0506; Sahin-Tóth, Miklós/0000-0003-4513-9922; Németh, Balázs/0000-0001-5338-7577}
}

@article{MTMT:33864451,
	title = {Detailed characteristics of post-discharge mortality in acute pancreatitis},
	url = {https://m2.mtmt.hu/api/publication/33864451},
	author = {Turcsiné Czapári, Dóra and Váradi, Alex and Borbásné Farkas, Kornélia and Nyári, Gergely Róbert and Márta, Katalin and Váncsa, Szilárd and Nagy, Rita and Teutsch, Brigitta and Bunduc, Stefania and Erőss, Bálint Mihály and Czakó, László and Vincze, Áron and Izbéki, Ferenc and Papp, Mária and Merkely, Béla Péter and Szentesi, Andrea Ildikó and Hegyi, Péter},
	doi = {10.1053/j.gastro.2023.05.028},
	journal-iso = {GASTROENTEROLOGY},
	journal = {GASTROENTEROLOGY},
	volume = {165},
	unique-id = {33864451},
	issn = {0016-5085},
	abstract = {The in-hospital survival of patients suffering from acute pancreatitis (AP) is 95-98%. However, there is growing evidence that patients discharged after AP may be at risk of serious morbidity and mortality. Here, we aimed to investigate the risk, causes, and predictors of the most severe consequence of the post-AP period: mortality.2,613, well-characterized patients from twenty-five centers were collected and followed by the Hungarian Pancreatic Study Group between 2012 and 2021. A general and a hospital-based population was used as the control group.After an AP episode patients have an approximately three-fold higher incidence rate of mortality than the general population (0.0404vs.0.0130 person-years). First-year mortality after discharge was almost double than in-hospital mortality (5.5%vs.3.5%), with 3.0% occurring in the first 90-day period. Age, comorbidities, and severity were the most significant independent risk factors for death following AP. Furthermore, multivariate analysis identified creatinine, glucose, and pleural fluid on admission as independent risk factors associated with post-discharge mortality. In the first 90-day period, cardiac failure and AP-related sepsis were among the main causes of death following discharge, while cancer-related cachexia and non-AP-related infection were the key causes in the later phase.Almost as many patients in our cohort die in the first 90-day period after discharge as during their hospital stay. Evaluation of cardiovascular status, follow-up of local complications, and cachexia-preventing oncological care should be an essential part of post-AP patient care. Future study protocols in AP must include at least a 90-day follow-up period after discharge.},
	year = {2023},
	eissn = {1528-0012},
	pages = {682-695},
	orcid-numbers = {Váradi, Alex/0000-0001-8229-6340; Borbásné Farkas, Kornélia/0000-0002-5349-6527; Márta, Katalin/0000-0002-2213-4865; Váncsa, Szilárd/0000-0002-9347-8163; Nagy, Rita/0000-0002-2663-4912; Teutsch, Brigitta/0000-0002-9530-7886; Erőss, Bálint Mihály/0000-0003-3658-8427; Czakó, László/0000-0002-6331-0802; Vincze, Áron/0000-0003-2217-7686; Izbéki, Ferenc/0000-0001-7767-4319; Papp, Mária/0000-0003-3662-4010; Merkely, Béla Péter/0000-0001-6514-0723; Szentesi, Andrea Ildikó/0000-0003-2097-6927; Hegyi, Péter/0000-0003-0399-7259; Imrei, Marcell/0000-0003-0175-7462; Németh, Balázs/0000-0001-5338-7577; Tiszlavicz, László/0000-0003-1134-6587; Oláh, Orsolya/0000-0002-5731-4030; Vitális, Zsuzsanna/0000-0001-8198-5312; Doros, Attila/0000-0002-6496-9895}
}

@article{MTMT:33813736,
	title = {The PANcreatic Disease ReseArch (PANDoRA) consortium : ten years' experience of association studies to understand the genetic architecture of pancreatic cancer},
	url = {https://m2.mtmt.hu/api/publication/33813736},
	author = {Campa, Daniele and Gentiluomo, Manuel and Stein, Angelika and Aoki, Mateus Nóbrega and Oliverius, Martin and Vodičková, Ludmila and Jamroziak, Krzysztof and Theodoropoulos, George and Pasquali, Claudio and Greenhalf, William and Arcidiacono, Paolo Giorgio and Uzunoglu, Faik and Pezzilli, Raffaele and Luchini, Claudio and Puzzono, Marta and Loos, Martin and Giaccherini, Matteo and Katzke, Verena and Mambrini, Andrea and Kiudeliene, Edita and Federico, Kauffmann Emanuele and Johansen, Julia and Hussein, Tamás and Mohelnikova-Duchonova, Beatrice and van Eijck, Casper H J and Brenner, Hermann and Farinella, Riccardo and Pérez, Juan Sainz and Lovecek, Martin and Büchler, Markus W and Hlavac, Viktor and Izbicki, Jakob R and Hackert, Thilo and Chammas, Roger and Zerbi, Alessandro and Lawlor, Rita and Felici, Alessio and Götz, Mara and Capurso, Gabriele and Ginocchi, Laura and Gazouli, Maria and Kupcinskas, Juozas and Cavestro, Giulia Martina and Vodicka, Pavel and Moz, Stefania and Neoptolemos, John P and Kunovsky, Lumir and Bojesen, Stig E and Carrara, Silvia and Gioffreda, Domenica and Morkunas, Egidijus and Abian, Olga and Bunduc, Stefania and Basso, Daniela and Boggi, Ugo and Wlodarczyk, Barbara and Szentesi, Andrea Ildikó and Vanella, Giuseppe and Chen, Inna and Bijlsma, Maarten F and Kiudelis, Vytautas and Landi, Stefano and Schöttker, Ben and Corradi, Chiara and Giese, Nathalia and Kaaks, Rudolf and Peduzzi, Giulia and Hegyi, Péter and Morelli, Luca and Furbetta, Niccolò and Soucek, Pavel and Latiano, Anna and Talar-Wojnarowska, Renata and Lindgaard, Sidsel C and Dijk, Frederike and Milanetto, Anna Caterina and Tavano, Francesca and Cervena, Klara and Erőss, Bálint Mihály and Testoni, Sabrina G and Verhagen-Oldenampsen, Judith H E and Małecka-Wojciesko, Ewa and Costello, Eithne and Salvia, Roberto and Maiello, Evaristo and Ermini, Stefano and Sperti, Cosimo and Holleczek, Bernd and Perri, Francesco and Skieceviciene, Jurgita and Archibugi, Livia and Lucchesi, Maurizio and Rizzato, Cosmeri and Canzian, Federico},
	doi = {10.1016/j.critrevonc.2023.104020},
	journal-iso = {CRIT REV ONCOL HEMAT},
	journal = {CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY},
	volume = {186},
	unique-id = {33813736},
	issn = {1040-8428},
	abstract = {Pancreatic cancer has an incidence that almost matches its mortality. Only a small number of risk factors and 33 susceptibility loci have been identified. so Moreover, the relative rarity of pancreatic cancer poses significant hurdles for research aimed at increasing our knowledge of the genetic mechanisms contributing to the disease. Additionally, the inability to adequately power research questions prevents small monocentric studies from being successful. Several consortia have been established to pursue a better understanding of the genetic architecture of pancreatic cancers. The Pancreatic disease research (PANDoRA) consortium is the largest in Europe. PANDoRA is spread across 12 European countries, Brazil and Japan, bringing together 29 basic and clinical research groups. In the last ten years, PANDoRA has contributed to the discovery of 25 susceptibility loci, a feat that will be instrumental in stratifying the population by risk and optimizing preventive strategies.},
	keywords = {chronic pancreatitis; Pancreatic cancer; Pancreatic ductal adenocarcinoma; Genetic epidemiology; PANCREATIC NEUROENDOCRINE TUMORS; CONSORTIUM; intraductal papillary mucinous neoplasms},
	year = {2023},
	eissn = {1879-0461},
	orcid-numbers = {Szentesi, Andrea Ildikó/0000-0003-2097-6927; Hegyi, Péter/0000-0003-0399-7259; Erőss, Bálint Mihály/0000-0003-3658-8427}
}