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2. All‐cause and liver‐related mortality risk factors in excessive drinkers: Analysis of data from the UK biobank

Author

Whitfield, John B, Seth, Devanshi, Morgan, Timothy R, Aithal, Guruprasad P, Atkinson, Stephen R, Bataller, Ramon, Botwin, Gregory, Chalasani, Naga P, Cordell, Heather J, Daly, Ann K, Darlay, Rebecca, Day, Christopher P, Eyer, Florian, Foroud, Tatiana, Gleeson, Dermot, Goldman, David, Haber, Paul S, Jacquet, Jean‐Marc, Liang, Tiebing, Liangpunsakul, Suthat, Masson, Steven, Mathurin, Philippe, Moirand, Romain, Moreno, Christophe, Morgan, Marsha Y, Mueller, Sebastian, Müllhaupt, Beat, Nagy, Laura E, Nahon, Pierre, Nalpas, Bertrand, Naveau, Sylvie, Perney, Pascal, Pirmohamed, Munir, Schwantes‐An, Tae‐Hwi, Seitz, Helmut K, Soyka, Michael, Stickel, Felix, Thompson, Andrew, Thursz, Mark R, and Trepo, Eric

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Digestive Diseases, Substance Misuse, Liver Disease, Nutrition, Brain Disorders, Alcoholism, Alcohol Use and Health, Clinical Research, Cancer, Oral and gastrointestinal, Good Health and Well Being, Humans, Male, Female, Alcoholism, Alcohol Drinking, Biological Specimen Banks, Risk Factors, Cardiovascular Diseases, Liver, United Kingdom, alcohol, alcohol dependence, all-cause mortality, excessive drinking, liver disease, GenomALC Consortium, Neurosciences, Psychology, Substance Abuse, Clinical sciences, Biological psychology, Clinical and health psychology
Abstract

BackgroundHigh alcohol intake is associated with increased mortality. We aimed to identify factors affecting mortality in people drinking extreme amounts of alcohol.MethodsWe obtained information from the UK Biobank on approximately 500,000 participants aged 40-70 years at baseline assessment in 2006-2010. Habitual alcohol intake, lifestyle and physiological data, laboratory test results, and hospital diagnoses and death certificate data (to June 2020) for 5136 men (2.20% of male participants) and 1504 women (0.60%) who reported consuming ≥80 or ≥50 g/day, respectively, were used in survival analysis.ResultsMortality hazard ratios for these excessive drinkers, compared to all other participants, were 2.02 (95% CI 1.89-2.17) for all causes, 1.89 (1.69-2.12) for any cancer, 1.87 (1.61-2.17) for any circulatory disease, and 9.40 (7.00-12.64) for any liver disease. Liver disease diagnosis or abnormal liver function tests predicted not only deaths attributed to liver disease but also those from cancers or circulatory diseases. Mortality among excessive drinkers was also associated with quantitative alcohol intake; diagnosed alcohol dependence, harmful use, or withdrawal syndrome; and current smoking at assessment.ConclusionsPeople with chronic excessive alcohol intake experience decreased average survival, but there is substantial variation in their mortality, with liver abnormality and alcohol dependence or other alcohol use disorders associated with a worse prognosis. Clinically, patients with these risk factors and high alcohol intake should be considered for early or intensive management. Research can usefully focus on the factors predisposing to dependence or liver abnormality.

Published
2022

3. A genetic risk score and diabetes predict development of alcohol-related cirrhosis in drinkers

Author

Whitfield, John B, Schwantes-An, Tae-Hwi, Darlay, Rebecca, Aithal, Guruprasad P, Atkinson, Stephen R, Bataller, Ramon, Botwin, Greg, Chalasani, Naga P, Cordell, Heather J, Daly, Ann K, Day, Christopher P, Eyer, Florian, Foroud, Tatiana, Gleeson, Dermot, Goldman, David, Haber, Paul S, Jacquet, Jean-Marc, Liang, Tiebing, Liangpunsakul, Suthat, Masson, Steven, Mathurin, Philippe, Moirand, Romain, McQuillin, Andrew, Moreno, Christophe, Morgan, Marsha Y, Mueller, Sebastian, Müllhaupt, Beat, Nagy, Laura E, Nahon, Pierre, Nalpas, Bertrand, Naveau, Sylvie, Perney, Pascal, Pirmohamed, Munir, Seitz, Helmut K, Soyka, Michael, Stickel, Felix, Thompson, Andrew, Thursz, Mark R, Trépo, Eric, Morgan, Timothy R, Seth, Devanshi, and Consortium, GenomALC

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Rare Diseases, Liver Cancer, Genetics, Liver Disease, Clinical Research, Substance Misuse, Genetic Testing, Cancer, Alcoholism, Alcohol Use and Health, Digestive Diseases, Chronic Liver Disease and Cirrhosis, Metabolic and endocrine, Oral and gastrointestinal, Good Health and Well Being, Adult, Alcohol Drinking, Case-Control Studies, Cohort Studies, Diabetes Mellitus, Female, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Liver Cirrhosis, Alcoholic, Male, Middle Aged, Polymorphism, Single Nucleotide, Risk Assessment, Hepatocellular carcinoma, risk stratification, chronic alcohol use, genome-wide association, single nucleotide polymorphism, coffee, GenomALC Consortium, Public Health and Health Services, Gastroenterology & Hepatology, Clinical sciences
Abstract

Background & aimsOnly a minority of excess alcohol drinkers develop cirrhosis. We developed and evaluated risk stratification scores to identify those at highest risk.MethodsThree cohorts (GenomALC-1: n = 1,690, GenomALC-2: n = 3,037, UK Biobank: relevant n = 6,898) with a history of heavy alcohol consumption (≥80 g/day (men), ≥50 g/day (women), for ≥10 years) were included. Cases were participants with alcohol-related cirrhosis. Controls had a history of similar alcohol consumption but no evidence of liver disease. Risk scores were computed from up to 8 genetic loci identified previously as associated with alcohol-related cirrhosis and 3 clinical risk factors. Score performance for the stratification of alcohol-related cirrhosis risk was assessed and compared across the alcohol-related liver disease spectrum, including hepatocellular carcinoma (HCC).ResultsA combination of 3 single nucleotide polymorphisms (SNPs) (PNPLA3:rs738409, SUGP1-TM6SF2:rs10401969, HSD17B13:rs6834314) and diabetes status best discriminated cirrhosis risk. The odds ratios (ORs) and (95% CIs) between the lowest (Q1) and highest (Q5) score quintiles of the 3-SNP score, based on independent allelic effect size estimates, were 5.99 (4.18-8.60) (GenomALC-1), 2.81 (2.03-3.89) (GenomALC-2), and 3.10 (2.32-4.14) (UK Biobank). Patients with diabetes and high risk scores had ORs of 14.7 (7.69-28.1) (GenomALC-1) and 17.1 (11.3-25.7) (UK Biobank) compared to those without diabetes and with low risk scores. Patients with cirrhosis and HCC had significantly higher mean risk scores than patients with cirrhosis alone (0.76 ± 0.06 vs. 0.61 ± 0.02, p = 0.007). Score performance was not significantly enhanced by information on additional genetic risk variants, body mass index or coffee consumption.ConclusionsA risk score based on 3 genetic risk variants and diabetes status enables the stratification of heavy drinkers based on their risk of cirrhosis, allowing for the provision of earlier preventative interventions.Lay summaryExcessive chronic drinking leads to cirrhosis in some people, but so far there is no way to identify those at high risk of developing this debilitating disease. We developed a genetic risk score that can identify patients at high risk. The risk of cirrhosis is increased >10-fold with just two risk factors - diabetes and a high genetic risk score. Risk assessment using this test could enable the early and personalised management of this disease in high-risk patients.

Published
2022

9. PSD3 downregulation confers protection against fatty liver disease

Author

Mancina, Rosellina M., Sasidharan, Kavitha, Lindblom, Anna, Wei, Ying, Ciociola, Ester, Jamialahmadi, Oveis, Pingitore, Piero, Andréasson, Anne-Christine, Pellegrini, Giovanni, Baselli, Guido, Männistö, Ville, Pihlajamäki, Jussi, Kärjä, Vesa, Grimaudo, Stefania, Marini, Ilaria, Maggioni, Marco, Becattini, Barbara, Tavaglione, Federica, Dix, Carly, Castaldo, Marie, Klein, Stephanie, Perelis, Mark, Pattou, Francois, Thuillier, Dorothée, Raverdy, Violeta, Dongiovanni, Paola, Fracanzani, Anna Ludovica, Stickel, Felix, Hampe, Jochen, Buch, Stephan, Luukkonen, Panu K., Prati, Daniele, Yki-Järvinen, Hannele, Petta, Salvatore, Xing, Chao, Schafmayer, Clemens, Aigner, Elmar, Datz, Christian, Lee, Richard G., Valenti, Luca, Lindén, Daniel, and Romeo, Stefano

Published
2022
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10. Evaluation of laboratory tests for cirrhosis and for alcohol use, in the context of alcoholic cirrhosis.

Author

Whitfield, John, Masson, Steven, Liangpunsakul, Suthat, Hyman, Jessica, Mueller, Sebastian, Aithal, Guruprasad, Eyer, Florian, Gleeson, Dermot, Thompson, Andrew, Stickel, Felix, Soyka, Michael, Daly, Ann, Cordell, Heather, Liang, Tiebing, Foroud, Tatiana, Lumeng, Lawrence, Pirmohamed, Munir, Nalpas, Bertrand, Bence, Camille, Jacquet, Jean-Marc, Louvet, Alexandre, Moirand, Romain, Nahon, Pierre, Naveau, Sylvie, Perney, Pascal, Podevin, Philippe, Haber, Paul, Seitz, Helmut, Day, Christopher, Mathurin, Philippe, Morgan, Timothy, and Seth, Devanshi

Subjects
Abstinence, Alcohol, Aspartate aminotransferase, Cirrhosis, Gamma glutamyl transferase, Adult, Alcohol Abstinence, Alcohol Drinking, Area Under Curve, Aspartate Aminotransferases, Bilirubin, Biomarkers, Case-Control Studies, Clinical Enzyme Tests, Europe, Female, Humans, International Normalized Ratio, Liver Cirrhosis, Alcoholic, Liver Function Tests, Male, Middle Aged, Predictive Value of Tests, ROC Curve, Reproducibility of Results, Risk Factors, Sex Factors, United States, gamma-Glutamyltransferase
Abstract

Laboratory tests can play an important role in assessment of alcoholic patients, including for evaluation of liver damage and as markers of alcohol intake. Evidence on test performance should lead to better selection of appropriate tests and improved interpretation of results. We compared laboratory test results from 1578 patients between cases (with alcoholic cirrhosis; 753 men, 243 women) and controls (with equivalent lifetime alcohol intake but no liver disease; 439 men, 143 women). Comparisons were also made between 631 cases who had reportedly been abstinent from alcohol for over 60 days and 364 who had not. ROC curve analysis was used to estimate and compare tests ability to distinguish patients with and without cirrhosis, and abstinent and drinking cases. The best tests for presence of cirrhosis were INR and bilirubin, with areas under the ROC curve (AUCs) of 0.91 ± 0.01 and 0.88 ± 0.01, respectively. Confining analysis to patients with no current or previous ascites gave AUCs of 0.88 ± 0.01 for INR and 0.85 ± 0.01 for bilirubin. GGT and AST showed discrimination between abstinence and recent drinking in patients with cirrhosis, including those without ascites, when appropriate (and for GGT, sex-specific) limits were used. For AST, a cut-off limit of 85 units/L gave 90% specificity and 37% sensitivity. For GGT, cut-off limits of 288 units/L in men and 138 units/L in women gave 90% specificity for both and 40% sensitivity in men, 63% sensitivity in women. INR and bilirubin show the best separation between patients with alcoholic cirrhosis (with or without ascites) and control patients with similar lifetime alcohol exposure. Although AST and GGT are substantially increased by liver disease, they can give useful information on recent alcohol intake in patients with alcoholic cirrhosis when appropriate cut-off limits are used.

Published
2018

11. Combined effects of PNPLA3, TM6SF2 and HSD17B13 variants on severity of biopsy-proven non-alcoholic fatty liver disease

Author

Paternostro, Rafael, Staufer, Katharina, Traussnigg, Stefan, Stättermayer, Albert-Friedrich, Halilbasic, Emina, Keritam, Omar, Meyer, Elias L., Stift, Judith, Wrba, Fritz, Sipos, Bence, Canbay, Ali, Schlattjan, Martin, Aigner, Elmar, Datz, Christian, Stickel, Felix, Schafmayer, Clemens, Hampe, Jochen, Buch, Stephan, Prager, Gerhard, Munda, Petra, Mandorfer, Mattias, Ferenci, Peter, and Trauner, Michael

Published
2021
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12. Rapid Response to Treatment of Autoimmune Hepatitis Associated With Remission at 6 and 12 Months

Author

Pape, Simon, Gevers, Tom J.G., Vrolijk, Jan Maarten, van Hoek, Bart, Bouma, Gerd, van Nieuwkerk, Carin M.J., Taubert, Richard, Jaeckel, Elmar, Manns, Michael P., Papp, Maria, Sipeki, Nora, Stickel, Felix, Efe, Cumali, Ozaslan, Ersan, Purnak, Tugrul, Nevens, Frederik, Kessener, Dominik J.N., Kahraman, Alisan, Wedemeyer, Heiner, Hartl, Johannes, Schramm, Christoph, Lohse, Ansgar W., Drenth, Joost P.H., and Heneghan, Michael A.

Published
2020
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14. Brief Report: Genetics of Alcoholic Cirrhosis—GenomALC Multinational Study

Author

Whitfield, John B, Rahman, Khairunnessa, Haber, Paul S, Day, Christopher P, Masson, Steven, Daly, Ann K, Cordell, Heather J, Mueller, Sebastian, Seitz, Helmut K, Liangpunsakul, Suthat, Westerhold, Chi, Liang, Tiebing, Lumeng, Lawrence, Foroud, Tatiana, Nalpas, Bertrand, Mathurin, Philippe, Stickel, Felix, Soyka, Michael, Botwin, Gregory J, Morgan, Timothy R, Seth, Devanshi, and Consortium, for the GenomALC

Subjects
Biomedical and Clinical Sciences, Biological Psychology, Clinical and Health Psychology, Clinical Sciences, Psychology, Liver Disease, Alcoholism, Alcohol Use and Health, Substance Misuse, Clinical Research, Chronic Liver Disease and Cirrhosis, Behavioral and Social Science, Digestive Diseases, Genetics, Aetiology, 2.1 Biological and endogenous factors, Oral and gastrointestinal, Good Health and Well Being, Alcohol Drinking, Australia, Case-Control Studies, Clinical Protocols, Family Health, France, Genome-Wide Association Study, Germany, Internationality, Liver Cirrhosis, Alcoholic, Patient Selection, Switzerland, United Kingdom, United States, GenomALC Consortium, Alcoholic Liver Disease, Cirrhosis, Genetic Risk Factors, Genomewide Association, High-Risk Drinkers, Neurosciences, Substance Abuse, Clinical sciences, Biological psychology, Clinical and health psychology
Abstract

BackgroundThe risk of alcohol-related liver cirrhosis increases with increasing alcohol consumption, but many people with very high intake escape from liver disease. We postulate that susceptibility to alcoholic cirrhosis has a complex genetic component and propose that this can be dissected through a large and sufficiently powered genomewide association study (GWAS).MethodsThe GenomALC Consortium comprises researchers from Australia, France, Germany, Switzerland, United Kingdom, and United States, with a joint aim of exploring the genetic and genomic basis of alcoholic cirrhosis. For this National Institutes of Health/National Institute on Alcohol Abuse and Alcoholism funded study, we are recruiting high-risk drinkers who are either cases (with alcoholic cirrhosis) or controls (drinking comparable amounts over similar time, but free of significant liver disease). Extensive phenotypic data are obtained using semistructured interviews and patient records, and blood samples are collected.ResultsWe have successfully recruited 859 participants including 538 matched case-control samples as of September 2014, using study-specific inclusion-exclusion criteria and data collection protocols. Of these, 580 are cases (442 men and 138 women) and 279 are controls (205 men and 74 women). Duration of excessive drinking was slightly greater in cases than controls and was significantly less in women than men. Cases had significantly lower lifetime alcohol intake than controls. Both cases and controls had a high prevalence of reported parental alcohol problems, but cases were significantly more likely to report that a father with alcohol problems had died from liver disease (odds ratio 2.53, 95% confidence interval 1.31 to 4.87, p = 0.0055).ConclusionsRecruitment of participants for a GWAS of alcoholic cirrhosis has proved feasible across countries with multiple sites. Affected patients often consume less alcohol than unaffected ones, emphasizing the existence of individual vulnerability factors. Cases are more likely to report liver disease in a father with alcohol problems than controls, consistent with a potential genetic component to the risk of alcoholic cirrhosis.

Published
2015

16. Liver Fibrosis and Metabolic Alterations in Adults With alpha-1-antitrypsin Deficiency Caused by the Pi*ZZ Mutation

Author

Hamesch, Karim, Mandorfer, Mattias, Pereira, Vítor M., Moeller, Linda S., Pons, Monica, Dolman, Grace E., Reichert, Matthias C., Schneider, Carolin V., Woditsch, Vivien, Voss, Jessica, Lindhauer, Cecilia, Fromme, Malin, Spivak, Igor, Guldiken, Nurdan, Zhou, Biaohuan, Arslanow, Anita, Schaefer, Benedikt, Zoller, Heinz, Aigner, Elmar, Reiberger, Thomas, Wetzel, Martin, Siegmund, Britta, Simões, Carolina, Gaspar, Rui, Maia, Luís, Costa, Dalila, Bento-Miranda, Mário, van Helden, Josef, Yagmur, Eray, Bzdok, Danilo, Stolk, Jan, Gleiber, Wolfgang, Knipel, Verena, Windisch, Wolfram, Mahadeva, Ravi, Bals, Robert, Koczulla, Rembert, Barrecheguren, Miriam, Miravitlles, Marc, Janciauskiene, Sabina, Stickel, Felix, Lammert, Frank, Liberal, Rodrigo, Genesca, Joan, Griffiths, William J., Trauner, Michael, Krag, Aleksander, Trautwein, Christian, and Strnad, Pavel

Published
2019
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18. Evaluation of laboratory tests for cirrhosis and for alcohol use, in the context of alcoholic cirrhosis

Author

Whitfield, John B., Masson, Steven, Liangpunsakul, Suthat, Hyman, Jessica, Mueller, Sebastian, Aithal, Guruprasad, Eyer, Florian, Gleeson, Dermot, Thompson, Andrew, Stickel, Felix, Soyka, Michael, Daly, Ann K., Cordell, Heather J., Liang, Tiebing, Foroud, Tatiana, Lumeng, Lawrence, Pirmohamed, Munir, Nalpas, Bertrand, Bence, Camille, Jacquet, Jean-Marc, Louvet, Alexandre, Moirand, Romain, Nahon, Pierre, Naveau, Sylvie, Perney, Pascal, Podevin, Philippe, Haber, Paul S., Seitz, Helmut K., Day, Christopher P., Mathurin, Philippe, Morgan, Timothy M., and Seth, Devanshi

Published
2018
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22. Alcoholic Cirrhosis and Hepatocellular Carcinoma

Author

Stickel, Felix, Cohen, Irun R., Series editor, Lajtha, N.S. Abel, Series editor, Paoletti, Rodolfo, Series editor, Lambris, John D., Series editor, Vasiliou, Vasilis, editor, Zakhari, Samir, editor, Seitz, Helmut K., editor, and Hoek, Jan B., editor

Published
2015
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23. Genetic variants in PNPLA3 and TM6SF2 predispose to the development of hepatocellular carcinoma in individuals with alcohol-related cirrhosis

Author

Stickel, Felix, Buch, Stephan, Nischalke, Hans Dieter, Weiss, Karl Heinz, Gotthardt, Daniel, Fischer, Janett, Rosendahl, Jonas, Marot, Astrid, Elamly, Mona, Casper, Markus, Lammert, Frank, McQuillin, Andrew, Zopf, Steffen, Spengler, Ulrich, Marhenke, Silke, Kirstein, Martha M., Vogel, Arndt, Eyer, Florian, von Felden, Johann, Wege, Henning, Buch, Thorsten, Schafmayer, Clemens, Braun, Felix, Deltenre, Pierre, Berg, Thomas, Morgan, Marsha Y., and Hampe, Jochen

Published
2018
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24. Geoepidemiology of Primary Biliary Cholangitis: Lessons from Switzerland

Author

Terziroli Beretta-Piccoli, Benedetta, Stirnimann, Guido, Cerny, Andreas, Semela, David, Hessler, Roxane, Helbling, Beat, Stickel, Felix, Kalid-de Bakker, Carolina, Bihl, Florian, Giostra, Emiliano, Filipowicz Sinnreich, Magdalena, Oneta, Carl, Baserga, Adriana, Invernizzi, Pietro, Carbone, Marco, and Mertens, Joachim

Published
2018
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27. Genetically determined expression of lipoprotein lipase is linked to hepatocellular carcinoma in alcohol-associated cirrhosis

Author

Schmalz, Franziska, additional, Fischer, Janett, additional, Innes, Hamish, additional, Buch, Stephan, additional, Möller, Christine, additional, Matz-Soja, Madlen, additional, Schönfels, Witigo V, additional, Kraemer, Benjamin, additional, Langhans, Bettina, additional, Klüners, Alexandra, additional, Soyka, Michael, additional, Stickel, Felix, additional, Nattermann, Jacob, additional, Strassburg, Christian, additional, Berg, Thomas, additional, Nischalke, Hans Dieter, additional, and Lutz, Philipp, additional

Published
2023
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29. Genetic Variation of SAMM50 Is Not an Independent Risk Factor for Alcoholic Hepatocellular Carcinoma in Caucasian Patients

Author

Nischalke, Hans Dieter, primary, Schmalz, Franziska, additional, Buch, Stephan, additional, Fischer, Janett, additional, Möller, Christine, additional, Matz-Soja, Madlen, additional, Krämer, Benjamin, additional, Langhans, Bettina, additional, Klüners, Alexandra, additional, Soyka, Michael, additional, Stickel, Felix, additional, Nattermann, Jacob, additional, Berg, Thomas, additional, Strassburg, Christian P., additional, and Lutz, Philipp, additional

Published
2022
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34. Epigenomic map of human liver reveals principles of zonated morphogenic and metabolic control

Author

Brosch, Mario, Kattler, Kathrin, Herrmann, Alexander, von Schönfels, Witigo, Nordström, Karl, Seehofer, Daniel, Damm, Georg, Becker, Thomas, Zeissig, Sebastian, Nehring, Sophie, Reichel, Fabian, Moser, Vincent, Thangapandi, Raghavan Veera, Stickel, Felix, Baretton, Gustavo, Röcken, Christoph, Muders, Michael, Matz-Soja, Madlen, Krawczak, Michael, Gasparoni, Gilles, Hartmann, Hella, Dahl, Andreas, Schafmayer, Clemens, Walter, Jörn, and Hampe, Jochen

Published
2018
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35. Genetic variation in TERT modifies the risk of hepatocellular carcinoma in alcohol-related cirrhosis: Results from a genome-wide case-control study

Author

Buch, Stephan, Innes, Hamish, Lutz, Philipp Ludwig, Nischalke, Hans Dieter, Marquardt, Jens U, Fischer, Janett, Weiss, Karl Heinz, Rosendahl, Jonas, Marot, Astrid, Krawczyk, Marcin, Casper, Markus, Lammert, Frank, Eyer, Florian, Vogel, Arndt, Marhenke, Silke, Von Felden, Johann, Sharma, Rohini, Atkinson, Stephen Rahul, McQuillin, Andrew, Nattermann, Jacob, Schafmayer, Clemens, Franke, Andre, Strassburg, Christian, Rietschel, Marcella, Altmann, Heidi, Sulk, Stefan, Thangapandi, Veera Raghavan, Brosch, Mario, Lackner, Carolin, Stauber, Rudolf E, Canbay, Ali, Link, Alexander, Reiberger, Thomas, Mandorfer, Mattias, Semmler, Georg, Scheiner, Bernhard, Datz, Christian, Romeo, Stefano, Ginanni Corradini, Stefano, Irving, William Lucien, Morling, Joanne R., Guha, Indra Neil, Barnes, Eleanor, Ansari, M. Azim, Quistrebert, Jocelyn, Valenti, Luca, Morgan, Marsha Yvonne, Trebicka, Jonel, Berg, Thomas, Deltenre, Pierre, Mueller, Sebastian, Hampe, Jochen, and Stickel, Felix

Subjects
Gastroenterology
Abstract

Objective: Hepatocellular carcinoma (HCC) often develops in patients with alcohol-related cirrhosis at an annual risk of up to 2.5%. Some host genetic risk factors have been identified but do not account for the majority of the variance in occurrence. This study aimed to identify novel susceptibility loci for the development of HCC in people with alcohol related cirrhosis. Design: Patients with alcohol-related cirrhosis and HCC (cases: n=1214) and controls without HCC (n=1866), recruited from Germany, Austria, Switzerland, Italy and the UK, were included in a two-stage genome-wide association study using a case-control design. A validation cohort of 1520 people misusing alcohol but with no evidence of liver disease was included to control for possible association effects with alcohol misuse. Genotyping was performed using the InfiniumGlobal Screening Array (V.24v2, Illumina) and the OmniExpress Array (V.24v1-0a, Illumina). Results: Associations with variants rs738409 in PNPLA3 and rs58542926 in TM6SF2 previously associated with an increased risk of HCC in patients with alcohol-related cirrhosis were confirmed at genome-wide significance. A novel locus rs2242652(A) in TERT (telomerase reverse transcriptase) was also associated with a decreased risk of HCC, in the combined meta-Analysis, at genome-wide significance (p=6.41×10-9, OR=0.61 (95% CI 0.52 to 0.70). This protective association remained significant after correction for sex, age, body mass index and type 2 diabetes (p=7.94×10-5, OR=0.63 (95% CI 0.50 to 0.79). Carriage of rs2242652(A) in TERT was associated with an increased leucocyte telomere length (p=2.12×10-44). Conclusion: This study identifies rs2242652 in TERT as a novel protective factor for HCC in patients with alcohol-related cirrhosis.

Published
2022

37. Genetic variation inTERTmodifies the risk of hepatocellular carcinoma in alcohol-related cirrhosis: results from a genome-wide case-control study

Author

Buch, Stephan, primary, Innes, Hamish, additional, Lutz, Philipp Ludwig, additional, Nischalke, Hans Dieter, additional, Marquardt, Jens U, additional, Fischer, Janett, additional, Weiss, Karl Heinz, additional, Rosendahl, Jonas, additional, Marot, Astrid, additional, Krawczyk, Marcin, additional, Casper, Markus, additional, Lammert, Frank, additional, Eyer, Florian, additional, Vogel, Arndt, additional, Marhenke, Silke, additional, von Felden, Johann, additional, Sharma, Rohini, additional, Atkinson, Stephen Rahul, additional, McQuillin, Andrew, additional, Nattermann, Jacob, additional, Schafmayer, Clemens, additional, Franke, Andre, additional, Strassburg, Christian, additional, Rietschel, Marcella, additional, Altmann, Heidi, additional, Sulk, Stefan, additional, Thangapandi, Veera Raghavan, additional, Brosch, Mario, additional, Lackner, Carolin, additional, Stauber, Rudolf E, additional, Canbay, Ali, additional, Link, Alexander, additional, Reiberger, Thomas, additional, Mandorfer, Mattias, additional, Semmler, Georg, additional, Scheiner, Bernhard, additional, Datz, Christian, additional, Romeo, Stefano, additional, Ginanni Corradini, Stefano, additional, Irving, William Lucien, additional, Morling, Joanne R, additional, Guha, Indra Neil, additional, Barnes, Eleanor, additional, Ansari, M Azim, additional, Quistrebert, Jocelyn, additional, Valenti, Luca, additional, Müller, Sascha A, additional, Morgan, Marsha Yvonne, additional, Dufour, Jean-François, additional, Trebicka, Jonel, additional, Berg, Thomas, additional, Deltenre, Pierre, additional, Mueller, Sebastian, additional, Hampe, Jochen, additional, and Stickel, Felix, additional

Published
2022
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38. Genetic variation in TERT modifies the risk of hepatocellular carcinoma in alcohol-related cirrhosis: results form a genome-wide case-control study

Author

Buch, Stephan, primary, Innes, Hamish, additional, Lutz, Philipp, additional, Nischalke, Hans Dieter, additional, Nattermann, Jacob, additional, Marquardt, Jens U., additional, Fischer, Janett, additional, Weiss, Karl Heinz, additional, Rosendahl, Jonas, additional, Marot, Astrid, additional, Krawczyk, Marcin, additional, Casper, Markus, additional, Lammert, Frank, additional, Eyer, Florian, additional, Vogel, Arndt, additional, Marhenke, Silke, additional, von Felden, Johann, additional, Sharma, Rohini, additional, Atkinson, Stephen, additional, McQuillin, Andrew, additional, Schafmayer, Clemens, additional, Strassburg, Christian, additional, Altmann, Heidi, additional, Sulk, Stefan, additional, Thangapandi, Veera Raghavan, additional, Brosch, Mario, additional, Lackner, Carolin, additional, Stauber, Rudolf E., additional, Canbay, Ali, additional, Link, Alexander, additional, Reiberger, Thomas, additional, Mandorfer, Mattias, additional, Semmler, Georg, additional, Scheiner, Bernhard, additional, Datz, Christian, additional, Romeo, Stefano, additional, Corradini, Stefano Ginanni, additional, Valenti, Luca, additional, Müller, Sascha, additional, Morgan, Marsha, additional, Dufour, Jean-Francois, additional, Trebicka, Jonel, additional, Berg, Thomas, additional, Deltenre, Pierre, additional, Mueller, Sebastian, additional, Hampe, Jochen, additional, and Stickel, Felix, additional

Published
2022
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40. A genetic risk score and diabetes predict development of alcohol-related cirrhosis in drinkers

Author

Whitfield, John B., Schwantes-An, Tae Hwi, Darlay, Rebecca, Aithal, Guruprasad P., Atkinson, Stephen R., Bataller, Ramon, Botwin, Greg, Chalasani, Naga P., Cordell, Heather J., Daly, Ann K., Day, Christopher P., Eyer, Florian, Foroud, Tatiana, Gleeson, Dermot, Goldman, David, Haber, Paul S., Jacquet, Jean Marc, Liang, Tiebing, Liangpunsakul, Suthat, Masson, Steven, Mathurin, Philippe, Moirand, Romain, McQuillin, Andrew, Moreno, Christophe, Morgan, Marsha Y., Mueller, Sebastian, Nagy, Laura E., Nahon, Pierre, Nalpas, Bertrand, Naveau, Sylvie, Perney, Pascal, Pirmohamed, Munir, Seitz, Helmut K., Soyka, Michael, Stickel, Felix, Thompson, Andrew, Thursz, Mark R., Tre?po, Eric, Morgan, Timothy R., and Seth, Devanshi

Subjects
genome wide association, Hepatocellular carcinoma, single nucleotide polymorphism, coffee, risk stratification, chronic alcohol use
Abstract

Background & Aims: Only a minority of excess alcohol drinkers develop cirrhosis. We developed and evaluated risk stratification scores to identify those at highest risk. Methods: Three cohorts (GenomALC-1: n = 1,690, GenomALC-2: n = 3,037, UK Biobank: relevant n = 6,898) with a history of heavy alcohol consumption (≥80 g/day (men), ≥50 g/day (women), for ≥10 years) were included. Cases were participants with alcohol-related cirrhosis. Controls had a history of similar alcohol consumption but no evidence of liver disease. Risk scores were computed from up to 8 genetic loci identified previously as associated with alcohol-related cirrhosis and 3 clinical risk factors. Score performance for the stratification of alcohol-related cirrhosis risk was assessed and compared across the alcohol-related liver disease spectrum, including hepatocellular carcinoma (HCC). Results: A combination of 3 single nucleotide polymorphisms (SNPs) (PNPLA3:rs738409, SUGP1-TM6SF2:rs10401969, HSD17B13:rs6834314) and diabetes status best discriminated cirrhosis risk. The odds ratios (ORs) and (95% CIs) between the lowest (Q1) and highest (Q5) score quintiles of the 3-SNP score, based on independent allelic effect size estimates, were 5.99 (4.18–8.60) (GenomALC-1), 2.81 (2.03–3.89) (GenomALC-2), and 3.10 (2.32–4.14) (UK Biobank). Patients with diabetes and high risk scores had ORs of 14.7 (7.69–28.1) (GenomALC-1) and 17.1 (11.3–25.7) (UK Biobank) compared to those without diabetes and with low risk scores. Patients with cirrhosis and HCC had significantly higher mean risk scores than patients with cirrhosis alone (0.76 ± 0.06 vs. 0.61 ± 0.02, p = 0.007). Score performance was not significantly enhanced by information on additional genetic risk variants, body mass index or coffee consumption. Conclusions: A risk score based on 3 genetic risk variants and diabetes status enables the stratification of heavy drinkers based on their risk of cirrhosis, allowing for the provision of earlier preventative interventions. Lay summary: Excessive chronic drinking leads to cirrhosis in some people, but so far there is no way to identify those at high risk of developing this debilitating disease. We developed a genetic risk score that can identify patients at high risk. The risk of cirrhosis is increased >10-fold with just two risk factors – diabetes and a high genetic risk score. Risk assessment using this test could enable the early and personalised management of this disease in high-risk patients.

Published
2022

41. Genetic variation in modifies the risk of hepatocellular carcinoma in alcohol-related cirrhosis: results from a genome-wide case-control study.

Author

UCL - SSS/IREC/MONT - Pôle Mont Godinne, UCL - (MGD) Service de gastro-entérologie, Buch, Stephan, Innes, Hamish, Lutz, Philipp Ludwig, Nischalke, Hans Dieter, Marquardt, Jens U, Fischer, Janett, Weiss, Karl Heinz, Rosendahl, Jonas, Marot, Astrid, Krawczyk, Marcin, Casper, Markus, Lammert, Frank, Eyer, Florian, Vogel, Arndt, Marhenke, Silke, von Felden, Johann, Sharma, Rohini, Atkinson, Stephen Rahul, McQuillin, Andrew, Nattermann, Jacob, Schafmayer, Clemens, Franke, Andre, Strassburg, Christian, Rietschel, Marcella, Altmann, Heidi, Sulk, Stefan, Thangapandi, Veera Raghavan, Brosch, Mario, Lackner, Carolin, Stauber, Rudolf E, Canbay, Ali, Link, Alexander, Reiberger, Thomas, Mandorfer, Mattias, Semmler, Georg, Scheiner, Bernhard, Datz, Christian, Romeo, Stefano, Ginanni Corradini, Stefano, Irving, William Lucien, Morling, Joanne R, Guha, Indra Neil, Barnes, Eleanor, Ansari, M Azim, Quistrebert, Jocelyn, Valenti, Luca, Müller, Sascha A, Morgan, Marsha Yvonne, Dufour, Jean-François, Trebicka, Jonel, Berg, Thomas, Deltenre, Pierre, Mueller, Sebastian, Hampe, Jochen, Stickel, Felix, UCL - SSS/IREC/MONT - Pôle Mont Godinne, UCL - (MGD) Service de gastro-entérologie, Buch, Stephan, Innes, Hamish, Lutz, Philipp Ludwig, Nischalke, Hans Dieter, Marquardt, Jens U, Fischer, Janett, Weiss, Karl Heinz, Rosendahl, Jonas, Marot, Astrid, Krawczyk, Marcin, Casper, Markus, Lammert, Frank, Eyer, Florian, Vogel, Arndt, Marhenke, Silke, von Felden, Johann, Sharma, Rohini, Atkinson, Stephen Rahul, McQuillin, Andrew, Nattermann, Jacob, Schafmayer, Clemens, Franke, Andre, Strassburg, Christian, Rietschel, Marcella, Altmann, Heidi, Sulk, Stefan, Thangapandi, Veera Raghavan, Brosch, Mario, Lackner, Carolin, Stauber, Rudolf E, Canbay, Ali, Link, Alexander, Reiberger, Thomas, Mandorfer, Mattias, Semmler, Georg, Scheiner, Bernhard, Datz, Christian, Romeo, Stefano, Ginanni Corradini, Stefano, Irving, William Lucien, Morling, Joanne R, Guha, Indra Neil, Barnes, Eleanor, Ansari, M Azim, Quistrebert, Jocelyn, Valenti, Luca, Müller, Sascha A, Morgan, Marsha Yvonne, Dufour, Jean-François, Trebicka, Jonel, Berg, Thomas, Deltenre, Pierre, Mueller, Sebastian, Hampe, Jochen, and Stickel, Felix

Abstract

Hepatocellular carcinoma (HCC) often develops in patients with alcohol-related cirrhosis at an annual risk of up to 2.5%. Some host genetic risk factors have been identified but do not account for the majority of the variance in occurrence. This study aimed to identify novel susceptibility loci for the development of HCC in people with alcohol related cirrhosis. Patients with alcohol-related cirrhosis and HCC (cases: n=1214) and controls without HCC (n=1866), recruited from Germany, Austria, Switzerland, Italy and the UK, were included in a two-stage genome-wide association study using a case-control design. A validation cohort of 1520 people misusing alcohol but with no evidence of liver disease was included to control for possible association effects with alcohol misuse. Genotyping was performed using the InfiniumGlobal Screening Array (V.24v2, Illumina) and the OmniExpress Array (V.24v1-0a, Illumina). Associations with variants rs738409 in and rs58542926 in previously associated with an increased risk of HCC in patients with alcohol-related cirrhosis were confirmed at genome-wide significance. A novel locus rs2242652(A) in (telomerase reverse transcriptase) was also associated with a decreased risk of HCC, in the combined meta-analysis, at genome-wide significance (p=6.41×10, OR=0.61 (95% CI 0.52 to 0.70). This protective association remained significant after correction for sex, age, body mass index and type 2 diabetes (p=7.94×10, OR=0.63 (95% CI 0.50 to 0.79). Carriage of rs2242652(A) in was associated with an increased leucocyte telomere length (p=2.12×10). This study identifies rs2242652 in as a novel protective factor for HCC in patients with alcohol-related cirrhosis.

Published
2022

42. Cardiovascular Risk Assessment by SCORE2 Predicts Risk for Colorectal Neoplasia and Tumor-Related Mortality

Author

Wernly, Sarah; https://orcid.org/0000-0001-9264-3115, Semmler, Georg; https://orcid.org/0000-0002-0411-166X, Völkerer, Andreas, Rezar, Richard; https://orcid.org/0000-0002-7118-501X, Datz, Leonora, Radzikowski, Konrad, Stickel, Felix, Aigner, Elmar, Niederseer, David, Wernly, Bernhard; https://orcid.org/0000-0003-4024-0220, Datz, Christian; https://orcid.org/0000-0001-7838-4532, Wernly, Sarah; https://orcid.org/0000-0001-9264-3115, Semmler, Georg; https://orcid.org/0000-0002-0411-166X, Völkerer, Andreas, Rezar, Richard; https://orcid.org/0000-0002-7118-501X, Datz, Leonora, Radzikowski, Konrad, Stickel, Felix, Aigner, Elmar, Niederseer, David, Wernly, Bernhard; https://orcid.org/0000-0003-4024-0220, and Datz, Christian; https://orcid.org/0000-0001-7838-4532

Abstract

OBJECTIVES The European Society of Cardiology endorsed SCORE2 to assess cardiovascular risk. The aim of this observational, retrospective study was to assess whether SCORE2 is associated with colorectal neoplasia in an asymptomatic screening population. Further, we evaluated if SCORE2 predicts tumor-related mortality. METHODS We included 3408 asymptomatic patients who underwent a screening colonoscopy. We calculated SCORE2 for each participant and stratified patients according to their predicted 10-year risk of cardiovascular disease: SCORE2 0-4.9%, SCORE2 5-9.9%, and SCORE2 ≥ 10%. We assessed the association between SCORE2 as a continuous variable, the presence of colorectal neoplasia using multilevel logistic regression, and SCORE2 and mortality using Cox regression. RESULTS In total, 1537 patients had a SCORE2 of 0-4.9%, 1235 a SCORE2 of 5-9.9%, and 636 a SCORE2 ≥ 10%. The respective rates of colorectal neoplasia were 20%, 37%, and 44%. SCORE2 was associated with the presence of any (OR 1.11 95%CI 1.09-1.12; p < 0.001) and advanced colorectal neoplasia (OR 1.06 95%CI 1.08-1.13; p < 0.001) in univariate analysis. After multivariable adjustment (age, sex, family history, and metabolic syndrome) a higher SCORE2 remained associated with higher odds for any (aOR 1.04 95%CI 1.02-1.06; p = 0.001) and advanced (aOR 1.06 95%CI 1.03-1.10; p < 0.001) colorectal neoplasia. SCORE2 was associated with both all-cause (HR 1.11 95%CI 1.09-1.14; p < 0.001) and tumor-related mortality (HR 1.10 95%CI 1.05-1.14; p < 0.001). CONCLUSIONS We found that SCORE2 is associated with the presence of colorectal neoplasia. Clinicians could kill two birds with one stone calculating SCORE2. In patients with a high SCORE2, screening colonoscopy aside from cardiovascular risk mitigation could improve outcomes.

Published
2022

46. Successful fourth line treatment of a relapse patient with chronic hepatitis C virus infection genotype 3a using sofosbuvir, glecaprevir/pibrentasvir, and ribavirin: a case report

Author

Bernhard, Benedikt, Stickel, Felix, and University of Zurich

Subjects
Cyclopropanes, medicine.medical_specialty, Aminoisobutyric Acids, Pyrrolidines, Daclatasvir, Genotype, Proline, Sofosbuvir, Lactams, Macrocyclic, Voxilaprevir, 610 Medicine & health, Hepacivirus, Antiviral Agents, Gastroenterology, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Leucine, Quinoxalines, Internal medicine, Ribavirin, medicine, Humans, 2715 Gastroenterology, 030212 general & internal medicine, Sulfonamides, business.industry, virus diseases, Hepatitis C, Glecaprevir, Hepatitis C, Chronic, Middle Aged, medicine.disease, digestive system diseases, Pibrentasvir, Treatment Outcome, 10219 Clinic for Gastroenterology and Hepatology, chemistry, Benzimidazoles, Drug Therapy, Combination, Female, 030211 gastroenterology & hepatology, Neoplasm Recurrence, Local, business, Viral load, medicine.drug
Abstract

Relapses after therapy with direct-acting antiviral agents (DAA) in chronic hepatitis C virus (HCV) infections are rare due to high efficacy of interferon-free therapy regimens. The presence of resistance-associated substitutions (RAS) in proteins targeted by therapy can lead to lower rates of sustained virological response (SVR) in patients receiving DAA-therapy, and little evidence exists as to how to treat these patients. We present a case of a multi-drug-resistant HCV-genotype-3a-infection in a 50-year-old female without confirmed cirrhosis but with advanced fibrosis (liver stiffness 11.6 kPa) and low viral load. Resistance testing revealed a Y93H mutation in the NS5A gene. Therapies using sofosbuvir and daclatasvir (1 The combination of sofosbuvir, glecaprevir/pibrentasvir and ribavirin could be a rescue therapy after previous relapses on DAA-therapy, especially in patients with relapse after therapy with sofosbuvir, velpatasvir, and voxilaprevir. Rückfälle nach einer Therapie mit direkt antiviral wirkenden Substanzen (DAA) bei Patienten mit chronischer Virushepatitis C (HCV) sind aufgrund der hohen Wirksamkeit dieser Therapeutika selten. Das Auftreten von resistenzassoziierten Substitutionen (RAS) in Proteinen, auf die die Therapie abzielt, kann eine anhaltende Viruselimination (SVR) verhindern, und es existiert wenig Evidenz dazu, wie diese Patienten anschließend behandelt werden sollten. Wir berichten von einer 50-jährigen Patientin mit einer therapieresistenten HCV-Genotyp-3a-Infektion ohne bestätigte Leberzirrhose, aber mit fortgeschrittener Fibrose (Lebersteifigkeit 11,6 kPa) und niedriger Viruslast. Resistenztestungen zeigten eine Y93H-Mutation im NS5A-Gen des Virus. Mehrere Therapieversuche mit Sofosbuvir und Daclatasvir (1.), Sofosbuvir, Velpatasvir und Ribavirin (2.) und mit Sofosbuvir, Velpatasvir und Voxilaprevir (3.) konnten kein SVR erreichen. Es ergaben sich keine Hinweise auf eine eingeschränkte Compliance, da es jeweils nach vier Wochen zu einer schnellen und über den Therapiezeitraum persistierenden Negativierung der Viruslast kam. Als letzte Alternative erhielt die Patientin eine 24-wöchige Therapie mit Sofosbuvir, Glecaprevir/Pibrentasvir und gewichtsadaptiert 1000 mg Ribavirin. Damit erreichte sie ein SVR, entwickelte aber ein hepatozelluläres Karzinom. Die Kombination von Sofosbuvir, Glecaprevir/Pibrentasvir und Ribavirin kann eine effektive Therapie nach Rückfällen auf eine vorherige DAA-Therapie darstellen, insbesondere, wenn ein SVR nach Gabe von Sofosbuvir, Velpatasvir und Voxilaprevir ausbleibt.

Published
2020

47. The rs429358 Locus in Apolipoprotein E Is Associated With Hepatocellular Carcinoma in Patients With Cirrhosis

Author

Innes, Hamish, Nischalke, Hans Dieter, Guha, Indra Neil, Weiss, Karl Heinz, Irving, Will, Gotthardt, Daniel, Barnes, Eleanor, Fischer, Janett, Ansari, M. Azim, Rosendahl, Jonas, Lin, Shang‐Kuan, Marot, Astrid, Pedergnana, Vincent, Casper, Markus, Benselin, Jennifer, Lammert, Frank, McLauchlan, John, Lutz, Philip L., Hamill, Victoria, Mueller, Sebastian, Morling, Joanne R., Semmler, Georg, Eyer, Florian, von Felden, Johann, Link, Alexander, Vogel, Arndt, Marquardt, Jens U., Sulk, Stefan, Trebicka, Jonel, Valenti, Luca, Datz, Christian, Reiberger, Thomas, Schafmayer, Clemens, Berg, Thomas, Deltenre, Pierre, Hampe, Jochen, Stickel, Felix, Buch, Stephan, UCL - SSS/IREC/MONT - Pôle Mont Godinne, and UCL - (MGD) Service de gastro-entérologie

Subjects
Liver Cirrhosis, Carcinoma, Hepatocellular, Hepatology, Liver Neoplasms, Membrane Proteins, SNP, Genomics, Hepatitis C, Polymorphism, Single Nucleotide, digestive system diseases, ddc, Chronic Liver Disease, Apolipoproteins E, Cirrhosis, Genetics, Humans, Genetic Predisposition to Disease, Liver cancer
Abstract

The host genetic background for hepatocellular carcinoma (HCC) is incompletely understood. We aimed to determine if four germline genetic polymorphisms, rs429358 in apolipoprotein E (APOE), rs2642438 in mitochondrial amidoxime reducing component 1 (MARC1), rs2792751 in glycerol‐3‐phosphate acyltransferase (GPAM), and rs187429064 in transmembrane 6 superfamily member 2 (TM6SF2), previously associated with progressive alcohol‐related and nonalcoholic fatty liver disease, are also associated with HCC. Four HCC case‐control data sets were constructed, including two mixed etiology data sets (UK Biobank and FinnGen); one hepatitis C virus (HCV) cohort (STOP‐HCV), and one alcohol‐related HCC cohort (Dresden HCC). The frequency of each variant was compared between HCC cases and cirrhosis controls (i.e., patients with cirrhosis without HCC). Population controls were also considered. Odds ratios (ORs) associations were calculated using logistic regression, adjusting for age, sex, and principal components of genetic ancestry. Fixed‐effect meta‐analysis was used to determine the pooled effect size across all data sets. Across four case‐control data sets, 2,070 HCC cases, 4,121 cirrhosis controls, and 525,779 population controls were included. The rs429358:C allele (APOE) was significantly less frequent in HCC cases versus cirrhosis controls (OR, 0.71; 95% confidence interval [CI], 0.61‐0.84; P = 2.9 × 10−5). Rs187429064:G (TM6SF2) was significantly more common in HCC cases versus cirrhosis controls and exhibited the strongest effect size (OR, 2.03; 95% CI, 1.45‐2.86; P = 3.1 × 10−6). In contrast, rs2792751:T (GPAM) was not associated with HCC (OR, 1.01; 95% CI, 0.90‐1.13; P = 0.89), whereas rs2642438:A (MARC1) narrowly missed statistical significance (OR, 0.91; 95% CI, 0.84‐1.00; P = 0.043). Conclusion: This study associates carriage of rs429358:C (APOE) with a reduced risk of HCC in patients with cirrhosis. Conversely, carriage of rs187429064:G in TM6SF2 is associated with an increased risk of HCC in patients with cirrhosis.

Published
2022
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49. Variants APOE (rs429358) and TM6SF2 (rs187429064) modify the risk of hepatocellular carcinoma

Author

Innes, Hamish, additional, Nischalke, HansDieter, additional, Weiss, KarlHeinz, additional, Gotthardt, Daniel, additional, Guha, Neil, additional, Barnes, Eleanor, additional, Irving, Will, additional, Fischer, Janett, additional, Rosendahl, Jonas, additional, Casper, Markus, additional, Lammert, Frank, additional, Lutz, PhilipL, additional, Mueller, Sebastian, additional, Semmler, Georg, additional, Eyer, Florian, additional, von Felden, Johann, additional, Link, Alexander, additional, Vogel, Arndt, additional, Marquardt, JensU, additional, Sulk, Stefan, additional, Datz, Christian, additional, Reiberger, Thomas, additional, Schafmayer, Clemens, additional, Berg, Thomas, additional, Hampe, Jochen, additional, Stickel, Felix, additional, and Buch, Stephan, additional

Published
2022
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