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4. Intensivtherapie bei akuter Pankreatitis

Author

Stecher, Stephanie-Susanne, Beyer, Georg, Antón, Sofía, Aghdassi, Ali Alexander, Scheiber, Jonas Adrian, Lerch, Markus M., Mayerle, Julia, Marx, Gernot, editor, Muhl, Elke, editor, Zacharowski, Kai, editor, and Zeuzem, Stefan, editor

Published
2024
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6. The impact of physiological stress conditions on protein structure and trypsin inhibition of serine protease inhibitor Kazal type 1 (SPINK1) and its N34S variant

Author

Buchholz, Ina, Nagel, Felix, Klein, Annelie, Wagh, Preshit R., Mahajan, Ujjwal M., Greinacher, Andreas, Lerch, Markus M., Mayerle, Julia, and Delcea, Mihaela

Subjects
Quantitative Biology - Biomolecules
Abstract

One of the most common mutations in the serine protease inhibitor Kazal type 1 (SPINK1) gene is the N34S variant which is strongly associated with chronic pancreatitis. Although it is assumed that N34S mutation constitutes a high-risk factor, the underlying pathologic mechanism is still unknown. In the present study, we investigated the impact of physiological stress factors on SPINK1 protein structure and trypsin inhibitor function using biophysical methods. Our circular dichroism spectroscopy data revealed differences in the secondary structure of SPINK1 and N34S mutant suggesting protein structural changes induced by the mutation as an impairment that could be disease-relevant. We further confirmed that both SPINK1 (KD of 0.15 +/- 0.06 nM) and its N34S variant (KD of 0.08 +/- 0.02 nM) have similar binding affinity and inhibitory effect towards trypsin as shown by surface plasmon resonance and trypsin inhibition assay studies, respectively. We found that stress conditions such as altered ion concentrations (i.e. potassium, calcium), temperature shifts, as well as environmental pH lead to insignificant differences in trypsin inhibition between SPINK1 and N34S mutant. However, we have shown that the environmental pH induces structural changes in both SPINK1 constructs in a different manner. Our findings suggest protein structural changes in the N34S variant as an impairment of SPINK1 and environmental pH shift as a trigger that could play a role in disease progression of pancreatitis.

Published
2020
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7. Large-scale association analyses identify host factors influencing human gut microbiome composition

Author

Kurilshikov, Alexander, Medina-Gomez, Carolina, Bacigalupe, Rodrigo, Radjabzadeh, Djawad, Wang, Jun, Demirkan, Ayse, Le Roy, Caroline I, Raygoza Garay, Juan Antonio, Finnicum, Casey T, Liu, Xingrong, Zhernakova, Daria V, Bonder, Marc Jan, Hansen, Tue H, Frost, Fabian, Rühlemann, Malte C, Turpin, Williams, Moon, Jee-Young, Kim, Han-Na, Lüll, Kreete, Barkan, Elad, Shah, Shiraz A, Fornage, Myriam, Szopinska-Tokov, Joanna, Wallen, Zachary D, Borisevich, Dmitrii, Agreus, Lars, Andreasson, Anna, Bang, Corinna, Bedrani, Larbi, Bell, Jordana T, Bisgaard, Hans, Boehnke, Michael, Boomsma, Dorret I, Burk, Robert D, Claringbould, Annique, Croitoru, Kenneth, Davies, Gareth E, van Duijn, Cornelia M, Duijts, Liesbeth, Falony, Gwen, Fu, Jingyuan, van der Graaf, Adriaan, Hansen, Torben, Homuth, Georg, Hughes, David A, Ijzerman, Richard G, Jackson, Matthew A, Jaddoe, Vincent WV, Joossens, Marie, Jørgensen, Torben, Keszthelyi, Daniel, Knight, Rob, Laakso, Markku, Laudes, Matthias, Launer, Lenore J, Lieb, Wolfgang, Lusis, Aldons J, Masclee, Ad AM, Moll, Henriette A, Mujagic, Zlatan, Qibin, Qi, Rothschild, Daphna, Shin, Hocheol, Sørensen, Søren J, Steves, Claire J, Thorsen, Jonathan, Timpson, Nicholas J, Tito, Raul Y, Vieira-Silva, Sara, Völker, Uwe, Völzke, Henry, Võsa, Urmo, Wade, Kaitlin H, Walter, Susanna, Watanabe, Kyoko, Weiss, Stefan, Weiss, Frank U, Weissbrod, Omer, Westra, Harm-Jan, Willemsen, Gonneke, Payami, Haydeh, Jonkers, Daisy MAE, Arias Vasquez, Alejandro, de Geus, Eco JC, Meyer, Katie A, Stokholm, Jakob, Segal, Eran, Org, Elin, Wijmenga, Cisca, Kim, Hyung-Lae, Kaplan, Robert C, Spector, Tim D, Uitterlinden, Andre G, Rivadeneira, Fernando, Franke, Andre, Lerch, Markus M, Franke, Lude, Sanna, Serena, D’Amato, Mauro, and Pedersen, Oluf

Subjects
Microbiology, Biological Sciences, Genetics, Human Genome, Biotechnology, Clinical Research, Digestive Diseases, Nutrition, 2.1 Biological and endogenous factors, Aetiology, Oral and gastrointestinal, Adolescent, Adult, Bifidobacterium, Child, Child, Preschool, Cohort Studies, Female, Gastrointestinal Microbiome, Genetic Variation, Genome-Wide Association Study, Humans, Lactase, Linkage Disequilibrium, Male, Mendelian Randomization Analysis, Metabolism, Quantitative Trait Loci, RNA, Ribosomal, 16S, Medical and Health Sciences, Developmental Biology, Agricultural biotechnology, Bioinformatics and computational biology
Abstract

To study the effect of host genetics on gut microbiome composition, the MiBioGen consortium curated and analyzed genome-wide genotypes and 16S fecal microbiome data from 18,340 individuals (24 cohorts). Microbial composition showed high variability across cohorts: only 9 of 410 genera were detected in more than 95% of samples. A genome-wide association study of host genetic variation regarding microbial taxa identified 31 loci affecting the microbiome at a genome-wide significant (P

Published
2021

9. Trans-ethnic and Ancestry-Specific Blood-Cell Genetics in 746,667 Individuals from 5 Global Populations

Author

Chen, Ming-Huei, Raffield, Laura M, Mousas, Abdou, Sakaue, Saori, Huffman, Jennifer E, Moscati, Arden, Trivedi, Bhavi, Jiang, Tao, Akbari, Parsa, Vuckovic, Dragana, Bao, Erik L, Zhong, Xue, Manansala, Regina, Laplante, Véronique, Chen, Minhui, Lo, Ken Sin, Qian, Huijun, Lareau, Caleb A, Beaudoin, Mélissa, Hunt, Karen A, Akiyama, Masato, Bartz, Traci M, Ben-Shlomo, Yoav, Beswick, Andrew, Bork-Jensen, Jette, Bottinger, Erwin P, Brody, Jennifer A, van Rooij, Frank JA, Chitrala, Kumaraswamynaidu, Cho, Kelly, Choquet, Hélène, Correa, Adolfo, Danesh, John, Di Angelantonio, Emanuele, Dimou, Niki, Ding, Jingzhong, Elliott, Paul, Esko, Tõnu, Evans, Michele K, Floyd, James S, Broer, Linda, Grarup, Niels, Guo, Michael H, Greinacher, Andreas, Haessler, Jeff, Hansen, Torben, Howson, Joanna MM, Huang, Qin Qin, Huang, Wei, Jorgenson, Eric, Kacprowski, Tim, Kähönen, Mika, Kamatani, Yoichiro, Kanai, Masahiro, Karthikeyan, Savita, Koskeridis, Fotis, Lange, Leslie A, Lehtimäki, Terho, Lerch, Markus M, Linneberg, Allan, Liu, Yongmei, Lyytikäinen, Leo-Pekka, Manichaikul, Ani, Martin, Hilary C, Matsuda, Koichi, Mohlke, Karen L, Mononen, Nina, Murakami, Yoshinori, Nadkarni, Girish N, Nauck, Matthias, Nikus, Kjell, Ouwehand, Willem H, Pankratz, Nathan, Pedersen, Oluf, Preuss, Michael, Psaty, Bruce M, Raitakari, Olli T, Roberts, David J, Rich, Stephen S, Rodriguez, Benjamin AT, Rosen, Jonathan D, Rotter, Jerome I, Schubert, Petra, Spracklen, Cassandra N, Surendran, Praveen, Tang, Hua, Tardif, Jean-Claude, Trembath, Richard C, Ghanbari, Mohsen, Völker, Uwe, Völzke, Henry, Watkins, Nicholas A, Zonderman, Alan B, Program, VA Million Veteran, Wilson, Peter WF, Li, Yun, Butterworth, Adam S, Gauchat, Jean-François, Chiang, Charleston WK, and Li, Bingshan

Subjects
Genetics, Good Health and Well Being, Asian People, Genome-Wide Association Study, HEK293 Cells, Humans, Interleukin-7, Mutation, Missense, Phenotype, Polymorphism, Single Nucleotide, White People, VA Million Veteran Program, interleukin-7, genetic architecture, fine-mapping, selective sweeps, polygenic trait score, phenome-wide association study, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

Most loci identified by GWASs have been found in populations of European ancestry (EUR). In trans-ethnic meta-analyses for 15 hematological traits in 746,667 participants, including 184,535 non-EUR individuals, we identified 5,552 trait-variant associations at p < 5 × 10-9, including 71 novel associations not found in EUR populations. We also identified 28 additional novel variants in ancestry-specific, non-EUR meta-analyses, including an IL7 missense variant in South Asians associated with lymphocyte count in vivo and IL-7 secretion levels in vitro. Fine-mapping prioritized variants annotated as functional and generated 95% credible sets that were 30% smaller when using the trans-ethnic as opposed to the EUR-only results. We explored the clinical significance and predictive value of trans-ethnic variants in multiple populations and compared genetic architecture and the effect of natural selection on these blood phenotypes between populations. Altogether, our results for hematological traits highlight the value of a more global representation of populations in genetic studies.

Published
2020

10. Intensivtherapie bei akuter Pankreatitis

Author

Stecher, Stephanie-Susanne, primary, Beyer, Georg, additional, Antón, Sofía, additional, Aghdassi, Ali Alexander, additional, Scheiber, Jonas Adrian, additional, Lerch, Markus M., additional, and Mayerle, Julia, additional

Published
2023
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12. Obese Individuals with and without Type 2 Diabetes Show Different Gut Microbial Functional Capacity and Composition.

Author

Thingholm, Louise, Rühlemann, Malte, Koch, Manja, Fuqua, Brie, Laucke, Guido, Boehm, Ruwen, Bang, Corinna, Franzosa, Eric, Hübenthal, Matthias, Rahnavard, Ali, Frost, Fabian, Lloyd-Price, Jason, Schirmer, Melanie, Lusis, Aldons, Vulpe, Chris, Lerch, Markus, Homuth, Georg, Kacprowski, Tim, Schmidt, Carsten, Nöthlings, Ute, Karlsen, Tom, Lieb, Wolfgang, Laudes, Matthias, Franke, Andre, and Huttenhower, Curtis

Subjects
dietary supplements, iron, magnesium, medication, metabolic disease, microbiome, nutrition, obesity, type 2 diabetes, Animals, Bacteria, Biodiversity, Diabetes Mellitus, Type 2, Diet, Dietary Supplements, Feces, Female, Gastrointestinal Microbiome, Germany, Humans, Iron, Magnesium, Male, Metabolic Diseases, Metagenomics, Mice, Mice, Inbred C57BL, Multivariate Analysis, Nutrition Assessment, Obesity, Serum
Abstract

Obesity and type 2 diabetes (T2D) are metabolic disorders that are linked to microbiome alterations. However, their co-occurrence poses challenges in disentangling microbial features unique to each condition. We analyzed gut microbiomes of lean non-diabetic (n = 633), obese non-diabetic (n = 494), and obese individuals with T2D (n = 153) from German population and metabolic disease cohorts. Microbial taxonomic and functional profiles were analyzed along with medical histories, serum metabolomics, biometrics, and dietary data. Obesity was associated with alterations in microbiome composition, individual taxa, and functions with notable changes in Akkermansia, Faecalibacterium, Oscillibacter, and Alistipes, as well as in serum metabolites that correlated with gut microbial patterns. However, microbiome associations were modest for T2D, with nominal increases in Escherichia/Shigella. Medications, including antihypertensives and antidiabetics, along with dietary supplements including iron, were significantly associated with microbiome variation. These results differentiate microbial components of these interrelated metabolic diseases and identify dietary and medication exposures to consider in future studies.

Published
2019

13. Disentangling the genetics of lean mass.

Author

Karasik, David, Zillikens, M, Hsu, Yi-Hsiang, Aghdassi, Ali, Akesson, Kristina, Amin, Najaf, Barroso, Inês, Bennett, David, Bertram, Lars, Bochud, Murielle, Borecki, Ingrid, Broer, Linda, Buchman, Aron, Byberg, Liisa, Campbell, Harry, Campos-Obando, Natalia, Cauley, Jane, Cawthon, Peggy, Chambers, John, Chen, Zhao, Cho, Nam, Choi, Hyung, Chou, Wen-Chi, Cummings, Steven, de Groot, Lisette, De Jager, Phillip, Demuth, Ilja, Diatchenko, Luda, Econs, Michael, Eiriksdottir, Gudny, Enneman, Anke, Eriksson, Joel, Eriksson, Johan, Estrada, Karol, Evans, Daniel, Feitosa, Mary, Fu, Mao, Gieger, Christian, Grallert, Harald, Gudnason, Vilmundur, Lenore, Launer, Hayward, Caroline, Hofman, Albert, Homuth, Georg, Huffman, Kim, Husted, Lise, Illig, Thomas, Ingelsson, Erik, Ittermann, Till, Jansson, John-Olov, Johnson, Toby, Biffar, Reiner, Jordan, Joanne, Jula, Antti, Karlsson, Magnus, Khaw, Kay-Tee, Kilpeläinen, Tuomas, Klopp, Norman, Kloth, Jacqueline, Koller, Daniel, Kooner, Jaspal, Kraus, William, Kritchevsky, Stephen, Kutalik, Zoltán, Kuulasmaa, Teemu, Kuusisto, Johanna, Laakso, Markku, Lahti, Jari, Langdahl, Bente, Lerch, Markus, Lewis, Joshua, Lill, Christina, Lind, Lars, Lindgren, Cecilia, Liu, Yongmei, Livshits, Gregory, Ljunggren, Östen, Loos, Ruth, Lorentzon, Mattias, Luan, Jianan, Luben, Robert, Malkin, Ida, McGuigan, Fiona, Medina-Gomez, Carolina, Meitinger, Thomas, Melhus, Håkan, Mellström, Dan, Michaëlsson, Karl, Mitchell, Braxton, Morris, Andrew, Mosekilde, Leif, Nethander, Maria, Newman, Anne, OConnell, Jeffery, Oostra, Ben, Orwoll, Eric, Palotie, Aarno, Peacock, Munro, Perola, Markus, and Peters, Annette

Subjects
ADAMTS Proteins, Absorptiometry, Photon, Adipose Tissue, Adolescent, Adult, Aged, Aged, 80 and over, Alpha-Ketoglutarate-Dependent Dioxygenase FTO, Body Composition, Body Fluid Compartments, Electric Impedance, Extracellular Matrix Proteins, Female, Genome-Wide Association Study, Humans, Male, Middle Aged, Muscle, Skeletal, Phenotype, Polymorphism, Single Nucleotide, RNA-Binding Proteins, Receptor, Melanocortin, Type 4, Versicans, White People, Young Adult
Abstract

BACKGROUND: Lean body mass (LM) plays an important role in mobility and metabolic function. We previously identified five loci associated with LM adjusted for fat mass in kilograms. Such an adjustment may reduce the power to identify genetic signals having an association with both lean mass and fat mass. OBJECTIVES: To determine the impact of different fat mass adjustments on genetic architecture of LM and identify additional LM loci. METHODS: We performed genome-wide association analyses for whole-body LM (20 cohorts of European ancestry with n = 38,292) measured using dual-energy X-ray absorptiometry) or bioelectrical impedance analysis, adjusted for sex, age, age2, and height with or without fat mass adjustments (Model 1 no fat adjustment; Model 2 adjustment for fat mass as a percentage of body mass; Model 3 adjustment for fat mass in kilograms). RESULTS: Seven single-nucleotide polymorphisms (SNPs) in separate loci, including one novel LM locus (TNRC6B), were successfully replicated in an additional 47,227 individuals from 29 cohorts. Based on the strengths of the associations in Model 1 vs Model 3, we divided the LM loci into those with an effect on both lean mass and fat mass in the same direction and refer to those as sumo wrestler loci (FTO and MC4R). In contrast, loci with an impact specifically on LM were termed body builder loci (VCAN and ADAMTSL3). Using existing available genome-wide association study databases, LM increasing alleles of SNPs in sumo wrestler loci were associated with an adverse metabolic profile, whereas LM increasing alleles of SNPs in body builder loci were associated with metabolic protection. CONCLUSIONS: In conclusion, we identified one novel LM locus (TNRC6B). Our results suggest that a genetically determined increase in lean mass might exert either harmful or protective effects on metabolic traits, depending on its relation to fat mass.

Published
2019

17. Toll-Like Receptor 1 Locus Re-examined in a Genome-Wide Association Study Update on Anti–Helicobacter pylori IgG Titers

Author

Lam, Suk Yee, Mommersteeg, Michiel C., Yu, Bingting, Broer, Linda, Spaander, Manon C.W., Frost, Fabian, Weiss, Stefan, Völzke, Henry, Lerch, Markus M., Schöttker, Ben, Zhang, Yan, Stocker, Hannah, Brenner, Hermann, Levy, Daniel, Hwang, Shih-Jen, Wood, Alexis C., Rich, Stephen S., Rotter, Jerome I., Taylor, Kent D., Tracy, Russell P., Kabagambe, Edmond K., Leja, Marcis, Klovins, Janis, Peculis, Raitis, Rudzite, Dace, Nikitina-Zake, Liene, Skenders, Girts, Rovite, Vita, Uitterlinden, André, Kuipers, Ernst J., Fuhler, Gwenny M., Homuth, Georg, and Peppelenbosch, Maikel P.

Published
2022
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18. Diagnosis and treatment of exocrine pancreatic insufficiency in chronic pancreatitis: An international expert survey and case vignette study

Author

Falconi, Massimo, Zou, Wen-Bin, Engjom, Trond, Ooi, Chee Y., Sutton, Robert, Frulloni, Luca, Neoptolemos, John, Wilcox, Charles, Miroslav, Vujasinovic, Trikudanathan, Guru, Liao, Zhuan, Hauge, Truls, Mössner, Joachim, Hoge, Chantal, Fockens, Paul, Mieog, Sven, Capurso, Gabriele, Cui, Yunfeng, de Madaria, Enrique, Distler, Marius, Aghdassi, Ali, Whitcomb, David C., Russell, Kylie, Beyer, Georg, Kunovsky, Lumír, Kwanten, Wilhelmus, Nava, Andrea Kazemi, Conlon, Kevin, Siriwardena, A.K., Paiella, Salvatore, Alconchel, Felipe, Marino, Marco Vito, de Meijer, Vincent E., Domingo, Carlos, Kleeff, Jorg, Lakshmanan, Aarti, Lie Chu, Michael Jen, Bouwense, Stefan, Nashidengo, Pueya Rashid, Konstantinos, Perivoliotis, Muttillo, Edoardo Maria, Umar, Garzali Ibrahim, Castro Santiago, Maria Jesus, Lopez-Lopez, Victor, Torri, Francesco, Schmelzle, Moritz, Ignatavicius, Povilas, Wicherts, Dennis, Gomes, Antonio, Machairas, Nikolaos A., Dorovinis, Panagiotis I., Serrablo, Alejandro, Soreide, Kjetil, Rahbari, Mohammad, Jie Chu, Michael Jen, Ptasnuka, Margarita, Petrulionis, Marius, Noel, Colin Byron, Castro, Ernest, Di Martino, Marcello, Recordare, Alfonso, Stättner, Stefan, Ausania, Fabio, Hartman, Vera, Roeyen, Geert, Egorov, Viacheslav, Vanagas, Tomas, Ebrahim, Mohamed, Arabadzhieva, Elena, Malleo, Giuseppe, Li, Liang, Adams, David, Oracz, Grzegorz, Nageshwar, Reddy D., Waldthaler, Alexander, Masamune, Atsushi, Drewes, Asbjorn Mohr, Amodio, Antonio, Tirkes, Temel, Srivastava, Anshu, Beilman, Gregory J., Berger, Zoltan, Lindkvist, Bjorn, Cavestro, Giulia Martina, Gariepy, Cheryl, Czakó, Laszlo, Di Leo, Milena, Sharma, Vishal, Lakhtakia, Sundeep, Rana, Surinder Singh, Duggan, Sinaed N., Kwon, Chang-Il, Phillips, Anna Evans, Forsmark, Christopher E., Gleeson, Ferga C., Lehman, Glen A., Greenhalf, William, Costamagna, Guido, Halloran, Christopher M., Friess, Helmut, Rasmussen, Henrik Hojgaard, Ikeura, Tsukasa, Haldorsen, Ingfrid S., Itoi, Takao, Izbicki, Jacob R., Windsor, John, Poulsen, Jakob Lykke, Frokjaer, Jens Brondum, Larino-Noia, Jose, Wang, Dan, Garcia, Julio Iglesias, Kalaitzakis, Evangelos, Wertheim-Tysarowska, Kararzyna, Kubota, Kensuke, Larusch, Jessica, Lerch, Markus M., Hu, Liang-Hao, Erkan, Mert, Machicado, Jorg D., Arvanitakis, Marianna, Buchler, Markus W., Levy, Marlon F., Heyman, Melvin B., Nojgaard, Camilla, Khashab, Mouen A., Delhaye, Myriam, Ogura, Takeshi, Okazaki, Kazuichi, Ghaneh, Paula, Banks, Peter A., Gupta, Pankaj, Papachristou, Georgios I., Michl, Patrick, Levy, Philippe, Pukitis, Aldis, Pezzilli, Raffaele, Baron, Ryan D., Amann, Stephen T., Schwarzenberg, Sarah Jane, Isaji, Shuiji, Olesen, Soren Schou, Novovic, Srdan, Hughes, Steven J., Werlin, Steven L., Gonska, Tanja, Gardner, Timothy B., Topazian, Mark D., Weiss, Frank Ulrich, Akshintala, Venakata S., Morinville, Veronique D., Rebours, Vinciane, Vincze, Aron, Singh, Vikesh K., Cui, Naiqiang, Zhang, Hong, Li, Zhao-shen, de Rijk, Florence E.M., van Veldhuisen, Charlotte L., Besselink, Marc G., van Hooft, Jeanin E., van Santvoort, Hjalmar C., van Geenen, Erwin J.M., Hegyi, Peter, Löhr, J-Matthias, Dominguez-Munoz, Juan E., de Jonge, Pieter Jan F., Bruno, Marco J., and Verdonk, Robert C.

Published
2022
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19. HLA-DRB1∗16 and -DQB1∗05 alleles are strongly associated with autoimmune pancreatitis in a cohort of hundred patients

Author

Goni, Elisabetta, Regel, Ivonne, Mahajan, Ujjwal Mukund, Amodio, Antonio, De Marchi, Giulia, Beyer, Georg, Zuppardo, Raffaella Alessia, Di Leo, Milena, Lanzillotta, Marco, Bonatti, Francesco, Kauke, Teresa, Dick, Andrea, Weiss, Frank Ulrich, Schönermarck, Ulf, Lerch, Markus M., Frulloni, Luca, Cavestro, Giulia Martina, and Mayerle, Julia

Published
2022
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24. Metabolic Biomarkers of Pancreatic Cancer

Author

Mahajan, Ujjwal Mukund, Li, Qi, Kamlage, Beate, Lerch, Markus M., Mayerle, Julia, Coleman, William B., Series Editor, Tsongalis, Gregory J., Series Editor, Michalski, Christoph W., editor, Rosendahl, Jonas, editor, Michl, Patrick, editor, and Kleeff, Jörg, editor

Published
2020
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27. Autorinnen und Autoren

Author

Abele-Horn, Marianne, primary, Amann, Bruno, additional, Aspöck, Christoph, additional, Barner, Dorina, additional, Barre, Felix, additional, Barth, Fritz, additional, Becker, Karsten, additional, Behrens-Baumann, Wolfgang, additional, Below, Harald, additional, Berens, Milena, additional, Blaschke, Sabine, additional, Bley, Ivonne, additional, Bockholdt, Britta, additional, Borg, Michael, additional, von der Brelie, Christian, additional, Bulitta, Clemens, additional, Caspari, Gregor, additional, Clauberg, Sigrid, additional, Danner, Bernhard, additional, Dietlein, Edeltrud, additional, Dietz, Birgit, additional, Dissemond, Joachim, additional, Durovic, Ana, additional, Ebbecke, Benjamin, additional, Eberlein, Thomas, additional, Eckmann, Christian, additional, Eggers, Maren, additional, Elstner, Matthias, additional, Engelhart, Steffen, additional, Ettl, Brigitte, additional, Ewert, Ralf, additional, Federspil, Philippe, additional, Fengler, Thomas, additional, Fleßa, Steffen, additional, Franke, Steffen, additional, Bondio, Mariacarla Gadebusch, additional, Gastmeier, Petra, additional, Gattringer, Rainer, additional, Gebel, Jürgen, additional, Girndt, Matthias, additional, Gleich, Sabine, additional, Graninger, Wolfgang, additional, Groß, Raoul, additional, Gründling, Matthias, additional, Hagel, Stefan, additional, Hamprecht, Klaus, additional, Harnoss, Julian-Camill, additional, Heckmann, Matthias, additional, Heeg, Peter, additional, Heidecke, Claus-Dieter, additional, Heine, Alexander, additional, Heppner, Hans Jürgen, additional, Heudorf, Ursel, additional, Holzhausen, Jan, additional, Hübner, Claudia, additional, Jabs, Jonas, additional, Jacobshagen, Anja, additional, Jäkel, Christian, additional, Jansen, Bernd, additional, Jatzwauk, Lutz, additional, Kalunga-Peters, André, additional, Kampf, Günter, additional, Kellner, Robert, additional, Kiefel, Volker, additional, Kindler, Stefan, additional, Kirsch, Gerhard, additional, Koch, Stefan, additional, Kohlmann, Thomas, additional, Kohnen, Wolfgang, additional, Kolbe, Claudia, additional, Koller, Walter, additional, Krämer, Irene, additional, Kranz, Jennifer, additional, Krause, Wolfgang, additional, Krey, Karl-Friedrich, additional, Krüger, William H., additional, Kucheryava, Nataliya, additional, Külpmann, Rüdiger, additional, Küster, Helmut, additional, Kuhn, Sven-Olaf, additional, Labs, Eckard, additional, Lafontaine, Jörg, additional, Leiß, Ottmar, additional, Lerch, Markus M., additional, Lippert, Hans, additional, Loczenski, Barbara, additional, Maidhof, Heinrich, additional, Maier, David, additional, Maier, Stefan, additional, Martiny, Heike, additional, Maschmeyer, Georg, additional, Mavridou, Kiriaki, additional, Mellmann, Alexander, additional, Metelmann, Hans-Robert, additional, Mett, Tobias R., additional, Meybohm, Patrick, additional, Meyer, Elisabeth, additional, Mielke, Martin, additional, Müller, Jan-Uwe, additional, von Müller, Lutz, additional, Mutters, Nico T., additional, Nauck, Friedemann, additional, Nienhaus, Albert, additional, Notbohm, Gert, additional, Novotny, Alexander, additional, Ossadnik, Michael, additional, Ostgathe, Christoph, additional, Papke, Roald, additional, Paul, Thomas, additional, Penne, Alexander, additional, Piechota, Hansjürgen, additional, Pilatz, Adrian, additional, Pitten, Frank-Albert, additional, Platz, Thomas, additional, Pleyer, Uwe, additional, Pochhammer, Julius, additional, Pohl, Marcus, additional, Reißhauer, Anett, additional, von Rheinbaben, Friedrich, additional, Rimek, Dagmar, additional, Ritter, Manuel, additional, Ruback, Sylvia, additional, Schneidewind, Laila, additional, Schroeder, Henry W.S., additional, Schulz-Schaeffer, Walter, additional, Schulz-Stübner, Sebastian, additional, Schulze, Marco H., additional, Schwierzeck, Vera, additional, Seebauer, Christian, additional, Seifert, Julia, additional, Seifert, Ulrike, additional, Siegmann, Silvester, additional, Slevogt, Hortense, additional, Sonntag, Hans-Günther, additional, Steinmann, Eike, additional, Steinmann, Jochen, additional, Streitenberg, Lada, additional, Suchomel, Miranda, additional, Thanheiser, Marc, additional, Trautmann, Matthias, additional, Vakil, Richard, additional, Viehöver, Sibylle, additional, Vogt, Peter M., additional, Vonberg, Ralf-Peter, additional, Vossebein, Lutz, additional, Wagenlehner, Florian, additional, Walger, Peter, additional, Weimann, Arved, additional, Wendt, Constanze, additional, Wendt, Michael, additional, Wicker, Sabine, additional, Widmer, Andreas, additional, Wilke, Michael, additional, Wiltfang, Jens, additional, Zacharowski, Kai, additional, Ziech, Patrick, additional, and Zygmunt, Marek, additional

Published
2022
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28. Erratum: Large meta-analysis of genome-wide association studies identifies five loci for lean body mass.

Author

Zillikens, M Carola, Demissie, Serkalem, Hsu, Yi-Hsiang, Yerges-Armstrong, Laura M, Chou, Wen-Chi, Stolk, Lisette, Livshits, Gregory, Broer, Linda, Johnson, Toby, Koller, Daniel L, Kutalik, Zoltán, Luan, Jian'an, Malkin, Ida, Ried, Janina S, Smith, Albert V, Thorleifsson, Gudmar, Vandenput, Liesbeth, Hua Zhao, Jing, Zhang, Weihua, Aghdassi, Ali, Åkesson, Kristina, Amin, Najaf, Baier, Leslie J, Barroso, Inês, Bennett, David A, Bertram, Lars, Biffar, Rainer, Bochud, Murielle, Boehnke, Michael, Borecki, Ingrid B, Buchman, Aron S, Byberg, Liisa, Campbell, Harry, Campos Obanda, Natalia, Cauley, Jane A, Cawthon, Peggy M, Cederberg, Henna, Chen, Zhao, Cho, Nam H, Jin Choi, Hyung, Claussnitzer, Melina, Collins, Francis, Cummings, Steven R, De Jager, Philip L, Demuth, Ilja, Dhonukshe-Rutten, Rosalie AM, Diatchenko, Luda, Eiriksdottir, Gudny, Enneman, Anke W, Erdos, Mike, Eriksson, Johan G, Eriksson, Joel, Estrada, Karol, Evans, Daniel S, Feitosa, Mary F, Fu, Mao, Garcia, Melissa, Gieger, Christian, Girke, Thomas, Glazer, Nicole L, Grallert, Harald, Grewal, Jagvir, Han, Bok-Ghee, Hanson, Robert L, Hayward, Caroline, Hofman, Albert, Hoffman, Eric P, Homuth, Georg, Hsueh, Wen-Chi, Hubal, Monica J, Hubbard, Alan, Huffman, Kim M, Husted, Lise B, Illig, Thomas, Ingelsson, Erik, Ittermann, Till, Jansson, John-Olov, Jordan, Joanne M, Jula, Antti, Karlsson, Magnus, Khaw, Kay-Tee, Kilpeläinen, Tuomas O, Klopp, Norman, Kloth, Jacqueline SL, Koistinen, Heikki A, Kraus, William E, Kritchevsky, Stephen, Kuulasmaa, Teemu, Kuusisto, Johanna, Laakso, Markku, Lahti, Jari, Lang, Thomas, Langdahl, Bente L, Launer, Lenore J, Lee, Jong-Young, Lerch, Markus M, Lewis, Joshua R, Lind, Lars, Lindgren, Cecilia, and Liu, Yongmei

Subjects
Epidemiology, Biological Sciences, Health Sciences, Genetics
Abstract

A correction to this article has been published and is linked from the HTML version of this article.

Published
2017

29. Large meta-analysis of genome-wide association studies identifies five loci for lean body mass.

Author

Zillikens, M Carola, Demissie, Serkalem, Hsu, Yi-Hsiang, Yerges-Armstrong, Laura M, Chou, Wen-Chi, Stolk, Lisette, Livshits, Gregory, Broer, Linda, Johnson, Toby, Koller, Daniel L, Kutalik, Zoltán, Luan, Jian'an, Malkin, Ida, Ried, Janina S, Smith, Albert V, Thorleifsson, Gudmar, Vandenput, Liesbeth, Hua Zhao, Jing, Zhang, Weihua, Aghdassi, Ali, Åkesson, Kristina, Amin, Najaf, Baier, Leslie J, Barroso, Inês, Bennett, David A, Bertram, Lars, Biffar, Rainer, Bochud, Murielle, Boehnke, Michael, Borecki, Ingrid B, Buchman, Aron S, Byberg, Liisa, Campbell, Harry, Campos Obanda, Natalia, Cauley, Jane A, Cawthon, Peggy M, Cederberg, Henna, Chen, Zhao, Cho, Nam H, Jin Choi, Hyung, Claussnitzer, Melina, Collins, Francis, Cummings, Steven R, De Jager, Philip L, Demuth, Ilja, Dhonukshe-Rutten, Rosalie AM, Diatchenko, Luda, Eiriksdottir, Gudny, Enneman, Anke W, Erdos, Mike, Eriksson, Johan G, Eriksson, Joel, Estrada, Karol, Evans, Daniel S, Feitosa, Mary F, Fu, Mao, Garcia, Melissa, Gieger, Christian, Girke, Thomas, Glazer, Nicole L, Grallert, Harald, Grewal, Jagvir, Han, Bok-Ghee, Hanson, Robert L, Hayward, Caroline, Hofman, Albert, Hoffman, Eric P, Homuth, Georg, Hsueh, Wen-Chi, Hubal, Monica J, Hubbard, Alan, Huffman, Kim M, Husted, Lise B, Illig, Thomas, Ingelsson, Erik, Ittermann, Till, Jansson, John-Olov, Jordan, Joanne M, Jula, Antti, Karlsson, Magnus, Khaw, Kay-Tee, Kilpeläinen, Tuomas O, Klopp, Norman, Kloth, Jacqueline SL, Koistinen, Heikki A, Kraus, William E, Kritchevsky, Stephen, Kuulasmaa, Teemu, Kuusisto, Johanna, Laakso, Markku, Lahti, Jari, Lang, Thomas, Langdahl, Bente L, Launer, Lenore J, Lee, Jong-Young, Lerch, Markus M, Lewis, Joshua R, Lind, Lars, Lindgren, Cecilia, and Liu, Yongmei

Subjects
Humans, Thinness, 17-Hydroxysteroid Dehydrogenases, Aldehyde Oxidoreductases, Extracellular Matrix Proteins, Body Composition, Phenotype, Polymorphism, Single Nucleotide, Quantitative Trait Loci, Regulatory Elements, Transcriptional, Versicans, Genome-Wide Association Study, Insulin Receptor Substrate Proteins, ADAMTS Proteins, Alpha-Ketoglutarate-Dependent Dioxygenase FTO, Human Genome, Genetics, 1.1 Normal biological development and functioning
Abstract

Lean body mass, consisting mostly of skeletal muscle, is important for healthy aging. We performed a genome-wide association study for whole body (20 cohorts of European ancestry with n = 38,292) and appendicular (arms and legs) lean body mass (n = 28,330) measured using dual energy X-ray absorptiometry or bioelectrical impedance analysis, adjusted for sex, age, height, and fat mass. Twenty-one single-nucleotide polymorphisms were significantly associated with lean body mass either genome wide (p

Published
2017

35. Analysis of GPRC6A variants in different pancreatitis etiologies

Author

Kaune, Tom, Ruffert, Claudia, Hesselbarth, Nico, Damm, Marko, Krug, Sebastian, Cardinal von Widdern, Julian, Masson, Emmanuelle, Chen, Jian-Min, Rebours, Vinciane, Buscail, Louis, Férec, Claude, Grützmann, Robert, te Morsche, Rene H.M., Drenth, Joost PH., Cavestro, Giulia Martina, Zuppardo, Raffaella Alessia, Saftoiu, Adrian, Malecka-Panas, Ewa, Głuszek, Stanislaw, Bugert, Peter, Lerch, Markus M., Sendler, Matthias, Weiss, Frank Ulrich, Zou, Wen-Bin, Deng, Shun-Jiang, Liao, Zhuan, Scholz, Markus, Kirsten, Holger, Hegyi, Peter, Witt, Heiko, Michl, Patrick, Griesmann, Heidi, and Rosendahl, Jonas

Published
2020
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36. International consensus guidelines on surveillance for pancreatic cancer in chronic pancreatitis. Recommendations from the working group for the international consensus guidelines for chronic pancreatitis in collaboration with the International Association of Pancreatology, the American Pancreatic Association, the Japan Pancreas Society, and European Pancreatic Club

Author

Greenhalf, William, Lévy, Philippe, Gress, Thomas, Rebours, Vinciane, Brand, Randall E., Pandol, Steve, Chari, Suresh, Jørgensen, Maiken Thyregod, Mayerle, Julia, Lerch, Markus M., Hegyi, Péter, Kleeff, Jörg, Castillo, Carlos Fernández-del, Isaji, Shuiji, Shimosegawa, Tooru, Sheel, Andrea, Halloran, Christopher M, Garg, Pramod, Takaori, Kyoichi, Besselink, Marc G., Forsmark, Chris E., Wilcox, C.Mel, Maisonneuve, Patrick, Yadav, Dhiraj, Whitcomb, David, and Neoptolemos, John

Published
2020
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37. International Consensus Guidelines for Risk Factors in Chronic Pancreatitis. Recommendations from the working group for the international consensus guidelines for chronic pancreatitis in collaboration with the International Association of Pancreatology, the American Pancreatic Association, the Japan Pancreas Society, and European Pancreatic Club

Author

Hegyi, Péter, Párniczky, Andrea, Lerch, Markus M., Sheel, Andrea R.G., Rebours, Vinciane, Forsmark, Chris E., Del Chiaro, Marco, Rosendahl, Jonas, de-Madaria, Enrique, Szücs, Ákos, Takaori, Kyoichi, Yadav, Dhiraj, Gheorghe, Cristian, Rakonczay, Zoltán, Jr., Molero, Xavier, Inui, Kazuo, Masamune, Atsushi, Fernandez-Del Castillo, Carlos, Shimosegawa, Tooru, Neoptolemos, John P., Whitcomb, David C., and Sahin-Tóth, Miklós

Published
2020
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40. Genome-wide association study in 8,956 German individuals identifies influence of ABO histo-blood groups on gut microbiome

Author

Rühlemann, Malte Christoph, Hermes, Britt Marie, Bang, Corinna, Doms, Shauni, Moitinho-Silva, Lucas, Thingholm, Louise Bruun, Frost, Fabian, Degenhardt, Frauke, Wittig, Michael, Kässens, Jan, Weiss, Frank Ulrich, Peters, Annette, Neuhaus, Klaus, Völker, Uwe, Völzke, Henry, Homuth, Georg, Weiss, Stefan, Grallert, Harald, Laudes, Matthias, Lieb, Wolfgang, Haller, Dirk, Lerch, Markus M., Baines, John F., and Franke, Andre

Published
2021
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42. Systematic microscopic analysis of retrieved stents from a patient with pancreatic necrosis

Author

Khaimov Valeria, Frost Fabian, Lerch Markus M., Senz Volkmar, Grabow Niels, and Schmitz Klaus-Peter

Subjects
pancreatic fluid collections, pancreatic necrosis, metal stent, plastic stent, double pigtail stent, Medicine
Abstract

Pancreatic fluid collections (PFCs) are a common complication associated with pancreatic injury. Drainage of a PFC is usually indicated if a patient becomes symptomatic with complications such as bacterial superinfection, septicaemia, fistulas, biliary obstruction or gastric outlet obstruction. Endoscopic ultrasound guided drainage is a well-established minimally invasive procedure to insert stents into a fluid collection, most prominently plastic double pigtail stents (DPSs) and lumen-apposing metal stents (LAMS). Both, DPSs and LAMSs have advantages and disadvantages that need to be considered before treatment. However, the main factors leading to failure of currently available stent systems are the relatively short patency period and bacterial superinfection. In this study, we subjected two broadly used pancreatic stents, a DPS and a LAMS Hot AXIOS stent, which were retrieved from the same patient, to a systematic morphological analysis by scanning electron microscopy in order to identify factors related to stent topography and geometry and potentially involved in stent failure. Results of this work will provide essential information for future innovations regarding the stent design for drainage of PFCs.

Published
2020
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45. Copy number variants in lipid metabolism genes are associated with gallstones disease in men

Author

Pérez-Palma, Eduardo, Bustos, Bernabé I., Lal, Dennis, Buch, Stephan, Azocar, Lorena, Toliat, Mohammad Reza, Lieb, Wolfgang, Franke, Andre, Hinz, Sebastian, Burmeister, Greta, von Shönfels, Witigo, Schafmayer, Clemens, Ahnert, Peter, Völzke, Henry, Völker, Uwe, Homuth, Georg, Lerch, Markus M., Puschel, Klaus, Gutiérrez, Rodrigo A., Hampe, Jochen, Nürnberg, Peter, Miquel, Juan Francisco, and De Ferrari, Giancarlo V.

Published
2020
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46. Acute Pancreatitis—Progress and Challenges

Author

Afghani, Elham, Pandol, Stephen J, Shimosegawa, Tooru, Sutton, Robert, Wu, Bechien U, Vege, Santhi Swaroop, Gorelick, Fred, Hirota, Morihisa, Windsor, John, Lo, Simon K, Freeman, Martin L, Lerch, Markus M, Tsuji, Yoshihisa, Melmed, Gil Y, Wassef, Wahid, and Mayerle, Julia

Subjects
Digestive Diseases, Acute Disease, American Medical Association, Biomarkers, Disease Progression, Humans, Japan, Pancreas, Pancreatitis, Prognosis, Severity of Illness Index, Societies, Medical, United States, acute pancreatitis, post-ERCP pancreatitis, treatment, CRAI, quality indicators, Clinical Sciences, Gastroenterology & Hepatology
Abstract

An international symposium entitled "Acute pancreatitis: progress and challenges" was held on November 5, 2014 at the Hapuna Beach Hotel, Big Island, Hawaii, as part of the 45th Anniversary Meeting of the American Pancreatic Association and the Japanese Pancreas Society. The course was organized and directed by Drs. Stephen Pandol, Tooru Shimosegawa, Robert Sutton, Bechien Wu, and Santhi Swaroop Vege. The symposium objectives were to: (1) highlight current issues in management of acute pancreatitis, (2) discuss promising treatments, (3) consider development of quality indicators and improved measures of disease activity, and (4) present a framework for international collaboration for development of new therapies. This article represents a compilation and adaptation of brief summaries prepared by speakers at the symposium with the purpose of broadly disseminating information and initiatives.

Published
2015

47. Lysosome associated membrane proteins maintain pancreatic acinar cell homeostasis: LAMP-2 deficient mice develop pancreatitis.

Author

Mareninova, Olga A, Sendler, Matthias, Malla, Sudarshan Ravi, Yakubov, Iskandar, French, Samuel W, Tokhtaeva, Elmira, Vagin, Olga, Oorschot, Viola, Lüllmann-Rauch, Renate, Blanz, Judith, Dawson, David, Klumperman, Judith, Lerch, Markus M, Mayerle, Julia, Gukovsky, Ilya, and Gukovskaya, Anna S

Subjects
amylase secretion, autophagy, cathepsin B, cerulein
Abstract

Background & aimsThe pathogenic mechanism of pancreatitis is poorly understood. Recent evidence implicates defective autophagy in pancreatitis responses; however, the pathways mediating impaired autophagy in pancreas remain largely unknown. Here, we investigate the role of lysosome associated membrane proteins (LAMPs) in pancreatitis.MethodsWe analyzed changes in LAMPs in experimental models and human pancreatitis, and the underlying mechanisms: LAMP de-glycosylation and degradation. LAMP cleavage by cathepsin B (CatB) was analyzed by mass spectrometry. We used mice deficient in LAMP-2 to assess its role in pancreatitis.ResultsPancreatic levels of LAMP-1 and LAMP-2 greatly decrease across various pancreatitis models and in human disease. Pancreatitis does not trigger LAMPs' bulk de-glycosylation, but induces their degradation via CatB-mediated cleavage of LAMP molecule close to the boundary between luminal and transmembrane domains. LAMP-2 null mice spontaneously develop pancreatitis that begins with acinar cell vacuolization due to impaired autophagic flux, and progresses to severe pancreas damage characterized by trypsinogen activation, macrophage-driven inflammation, and acinar cell death. LAMP-2 deficiency causes a decrease in pancreatic digestive enzymes content, stimulates the basal and inhibits CCK-induced amylase secretion by acinar cells. The effects of LAMP-2 knockout and acute cerulein pancreatitis overlap, which corroborates the pathogenic role of LAMP decrease in experimental pancreatitis models.ConclusionsThe results indicate a critical role for LAMPs, particularly LAMP-2, in maintaining pancreatic acinar cell homeostasis, and provide evidence that defective lysosomal function, resulting in impaired autophagy, leads to pancreatitis. Mice with LAMP-2 deficiency present a novel genetic model of human pancreatitis caused by lysosomal/autophagic dysfunction.

Published
2015

48. Lysosome-Associated Membrane Proteins (LAMP) Maintain Pancreatic Acinar Cell Homeostasis: LAMP-2–Deficient Mice Develop Pancreatitis

Author

Mareninova, Olga A, Sendler, Matthias, Malla, Sudarshan Ravi, Yakubov, Iskandar, French, Samuel W, Tokhtaeva, Elmira, Vagin, Olga, Oorschot, Viola, Lüllmann-Rauch, Renate, Blanz, Judith, Dawson, David, Klumperman, Judith, Lerch, Markus M, Mayerle, Julia, Gukovsky, Ilya, and Gukovskaya, Anna S

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Biological Sciences, Digestive Diseases, 2.1 Biological and endogenous factors, Aetiology, Oral and gastrointestinal, Amylase Secretion, Autophagy, Cathepsin B, Cerulein, amylase secretion, autophagy, cathepsin B, cerulein, Biochemistry and cell biology, Clinical sciences
Abstract

Background & aimsThe pathogenic mechanism of pancreatitis is poorly understood. Recent evidence implicates defective autophagy in pancreatitis responses; however, the pathways mediating impaired autophagy in pancreas remain largely unknown. Here, we investigate the role of lysosome associated membrane proteins (LAMPs) in pancreatitis.MethodsWe analyzed changes in LAMPs in experimental models and human pancreatitis, and the underlying mechanisms: LAMP de-glycosylation and degradation. LAMP cleavage by cathepsin B (CatB) was analyzed by mass spectrometry. We used mice deficient in LAMP-2 to assess its role in pancreatitis.ResultsPancreatic levels of LAMP-1 and LAMP-2 greatly decrease across various pancreatitis models and in human disease. Pancreatitis does not trigger LAMPs' bulk de-glycosylation, but induces their degradation via CatB-mediated cleavage of LAMP molecule close to the boundary between luminal and transmembrane domains. LAMP-2 null mice spontaneously develop pancreatitis that begins with acinar cell vacuolization due to impaired autophagic flux, and progresses to severe pancreas damage characterized by trypsinogen activation, macrophage-driven inflammation, and acinar cell death. LAMP-2 deficiency causes a decrease in pancreatic digestive enzymes content, stimulates the basal and inhibits CCK-induced amylase secretion by acinar cells. The effects of LAMP-2 knockout and acute cerulein pancreatitis overlap, which corroborates the pathogenic role of LAMP decrease in experimental pancreatitis models.ConclusionsThe results indicate a critical role for LAMPs, particularly LAMP-2, in maintaining pancreatic acinar cell homeostasis, and provide evidence that defective lysosomal function, resulting in impaired autophagy, leads to pancreatitis. Mice with LAMP-2 deficiency present a novel genetic model of human pancreatitis caused by lysosomal/autophagic dysfunction.

Published
2015

49. Early detection of sporadic pancreatic cancer: summative review.

Author

Chari, Suresh T, Kelly, Kimberly, Hollingsworth, Michael A, Thayer, Sarah P, Ahlquist, David A, Andersen, Dana K, Batra, Surinder K, Brentnall, Teresa A, Canto, Marcia, Cleeter, Deborah F, Firpo, Matthew A, Gambhir, Sanjiv Sam, Go, Vay Liang W, Hines, O Joe, Kenner, Barbara J, Klimstra, David S, Lerch, Markus M, Levy, Michael J, Maitra, Anirban, Mulvihill, Sean J, Petersen, Gloria M, Rhim, Andrew D, Simeone, Diane M, Srivastava, Sudhir, Tanaka, Masao, Vinik, Aaron I, and Wong, David

Subjects
Humans, Carcinoma, Pancreatic Ductal, Pancreatic Neoplasms, Diagnostic Imaging, Biopsy, Prognosis, Molecular Diagnostic Techniques, Survival Analysis, Predictive Value of Tests, Interdisciplinary Communication, Cooperative Behavior, Biomedical Research, International Cooperation, Diffusion of Innovation, Congresses as Topic, Early Detection of Cancer, Biomarkers, Tumor, biomarker, diabetes, screening, familial, imaging, pancreatic ductal adenocarcinoma, Rare Diseases, Pancreatic Cancer, Cancer, Prevention, Digestive Diseases, 4.1 Discovery and preclinical testing of markers and technologies, Detection, screening and diagnosis, Clinical Sciences, Gastroenterology & Hepatology
Abstract

Pancreatic cancer (PC) is estimated to become the second leading cause of cancer death in the United States by 2020. Early detection is the key to improving survival in PC. Addressing this urgent need, the Kenner Family Research Fund conducted the inaugural Early Detection of Sporadic Pancreatic Cancer Summit Conference in 2014 in conjunction with the 45th Anniversary Meeting of the American Pancreatic Association and Japan Pancreas Society. This seminal convening of international representatives from science, practice, and clinical research was designed to facilitate challenging interdisciplinary conversations to generate innovative ideas leading to the creation of a defined collaborative strategic pathway for the future of the field. An in-depth summary of current efforts in the field, analysis of gaps in specific areas of expertise, and challenges that exist in early detection is presented within distinct areas of inquiry: Case for Early Detection: Definitions, Detection, Survival, and Challenges; Biomarkers for Early Detection; Imaging; and Collaborative Studies. In addition, an overview of efforts in familial PC is presented in an addendum to this article. It is clear from the summit deliberations that only strategically designed collaboration among investigators, institutions, and funders will lead to significant progress in early detection of sporadic PC.

Published
2015

50. Approaching Pancreatic Cancer Phenotypes via Metabolomics

Author

McGranaghan, Peter, Rennefahrt, Ulrike, Kamlage, Beate, Reszka, Regina, Schatz, Philipp, Bethan, Bianca, Mayerle, Julia, Lerch, Markus M., Neoptolemos, John, Section Editor, Urrutia, Raul A., Section Editor, Abbruzzese, James L., Section Editor, Büchler, Markus W., Section Editor, Neoptolemos, John P., editor, Urrutia, Raul, editor, Abbruzzese, James L., editor, and Büchler, Markus W., editor

Published
2018
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