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Epidemiological trends in incidence and mortality of hepatobiliary cancers in Germany.

https://arctichealth.org/en/permalink/ahliterature101653
Source
Scand J Gastroenterol. 2011 Sep;46(9):1092-8
Publication Type
Article
Date
Sep-2011
Author
Thomas von Hahn
Sandra Ciesek
Gerd Wegener
Ruben R Plentz
Tobias J Weismüller
Heiner Wedemeyer
Michael P Manns
Tim F Greten
Nisar P Malek
Author Affiliation
Department of Gastroenterology, Hepatology and Endocrinology , Medizinische Hochschule, Hannover Medical School, Hannover , Germany.
Source
Scand J Gastroenterol. 2011 Sep;46(9):1092-8
Date
Sep-2011
Language
English
Publication Type
Article
Abstract
Abstract Objective. While marked changes in the frequency of hepatobiliary malignancies, most notably hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC), have been observed in different populations, no such data have been reported for Germany. We aimed to provide epidemiological data on recent trends in liver-related mortality, specifically mortality from hepatobiliary malignancies, in Germany. Material and methods. We used incidence and mortality data to determine changes in the frequency of malignant and non-malignant liver disease in Germany over the past 30 years. Results. While overall liver disease mortality has slightly declined in Germany, deaths from hepatobiliary malignancies have declined in women, but remained constant in men. Among hepatobiliary malignancies, ICC stands out, because mortality has more than tripled both in men and women between 1998 and 2008. This is mirrored by a marked increase in new cases reported to local cancer registries, that is, incidence. Over the same time period, HCC and extrahepatic cholangiocarcinoma (ECC) have remained largely constant while gall bladder cancers (GBC) have declined twofold. The rapid rise in ICC is in line with finding from different regions worldwide, but in contrast to recent data from Denmark and France, two of Germany's direct neighbors. Conclusions. The incidence of and mortality from ICC are rising markedly in Germany. The risk factors underlying this trend are as yet unclear.
PubMed ID
21692710 View in PubMed
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Genome-wide association analysis in primary sclerosing cholangitis and ulcerative colitis identifies risk loci at GPR35 and TCF4.

https://arctichealth.org/en/permalink/ahliterature122406
Source
Hepatology. 2013 Sep;58(3):1074-83
Publication Type
Article
Date
Sep-2013
Author
David Ellinghaus
Trine Folseraas
Kristian Holm
Eva Ellinghaus
Espen Melum
Tobias Balschun
Jon K Laerdahl
Alexey Shiryaev
Daniel N Gotthardt
Tobias J Weismüller
Christoph Schramm
Michael Wittig
Annika Bergquist
Einar Björnsson
Hanns-Ulrich Marschall
Morten Vatn
Andreas Teufel
Christian Rust
Christian Gieger
H-Erich Wichmann
Heiko Runz
Martina Sterneck
Christian Rupp
Felix Braun
Rinse K Weersma
Cisca Wijmenga
Cyriel Y Ponsioen
Christopher G Mathew
Paul Rutgeerts
Séverine Vermeire
Erik Schrumpf
Johannes R Hov
Michael P Manns
Kirsten M Boberg
Stefan Schreiber
Andre Franke
Tom H Karlsen
Author Affiliation
Institute of Clinical Molecular Biology, Christian-Albrechts-University, Kiel, Germany.
Source
Hepatology. 2013 Sep;58(3):1074-83
Date
Sep-2013
Language
English
Publication Type
Article
Keywords
Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - genetics
Belgium
Case-Control Studies
Cholangitis, Sclerosing - epidemiology - ethnology - genetics
Colitis, Ulcerative - epidemiology - ethnology - genetics
Comorbidity
Genetic Loci - genetics
Genetic Predisposition to Disease - ethnology - genetics
Genome-Wide Association Study
Genotype
Germany
Great Britain
Humans
Netherlands
Norway
Polymorphism, Single Nucleotide - genetics
Receptors, G-Protein-Coupled - genetics
Risk factors
Transcription Factors - genetics
Abstract
Approximately 60%-80% of patients with primary sclerosing cholangitis (PSC) have concurrent ulcerative colitis (UC). Previous genome-wide association studies (GWAS) in PSC have detected a number of susceptibility loci that also show associations in UC and other immune-mediated diseases. We aimed to systematically compare genetic associations in PSC with genotype data in UC patients with the aim of detecting new susceptibility loci for PSC. We performed combined analyses of GWAS for PSC and UC comprising 392 PSC cases, 987 UC cases, and 2,977 controls and followed up top association signals in an additional 1,012 PSC cases, 4,444 UC cases, and 11,659 controls. We discovered novel genome-wide significant associations with PSC at 2q37 [rs3749171 at G-protein-coupled receptor 35 (GPR35); P = 3.0 × 10(-9) in the overall study population, combined odds ratio [OR] and 95% confidence interval [CI] of 1.39 (1.24-1.55)] and at 18q21 [rs1452787 at transcription factor 4 (TCF4); P = 2.61 × 10(-8) , OR (95% CI) = 0.75 (0.68-0.83)]. In addition, several suggestive PSC associations were detected. The GPR35 rs3749171 is a missense single nucleotide polymorphism resulting in a shift from threonine to methionine. Structural modeling showed that rs3749171 is located in the third transmembrane helix of GPR35 and could possibly alter efficiency of signaling through the GPR35 receptor.
By refining the analysis of a PSC GWAS by parallel assessments in a UC GWAS, we were able to detect two novel risk loci at genome-wide significance levels. GPR35 shows associations in both UC and PSC, whereas TCF4 represents a PSC risk locus not associated with UC. Both loci may represent previously unexplored aspects of PSC pathogenesis.
PubMed ID
22821403 View in PubMed
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No Evidence That Azathioprine Increases Risk of Cholangiocarcinoma in Patients With Primary Sclerosing Cholangitis.

https://arctichealth.org/en/permalink/ahliterature284952
Source
Clin Gastroenterol Hepatol. 2016 Dec;14(12):1806-1812
Publication Type
Article
Date
Dec-2016
Author
Roman Zenouzi
Tobias J Weismüller
Kristin K Jørgensen
Michael Bubenheim
Henrike Lenzen
Peter Hübener
Kornelius Schulze
Christina Weiler-Normann
Marcial Sebode
Hanno Ehlken
Nadine Pannicke
Johannes Hartl
Moritz Peiseler
Sina Hübener
Tom H Karlsen
Kirsten M Boberg
Michael P Manns
Ansgar W Lohse
Christoph Schramm
Source
Clin Gastroenterol Hepatol. 2016 Dec;14(12):1806-1812
Date
Dec-2016
Language
English
Publication Type
Article
Keywords
Adult
Azathioprine - adverse effects - therapeutic use
Cholangiocarcinoma - chemically induced - epidemiology
Cholangitis, Sclerosing - complications - drug therapy
Female
Germany - epidemiology
Humans
Immunosuppressive Agents - adverse effects - therapeutic use
Male
Middle Aged
Norway - epidemiology
Retrospective Studies
Risk assessment
Tertiary Care Centers
Young Adult
Abstract
Patients with primary sclerosing cholangitis (PSC) are at increased risk for developing cholangiocarcinoma (CCA). Patients with PSC also can have inflammatory bowel diseases (IBDs) or features of autoimmune hepatitis (AIH), and therefore are treated with azathioprine. Azathioprine has been associated with an increased risk for malignancy, therefore we investigated whether azathioprine use affects the risk of CCA in persons with PSC.
We performed a retrospective study of well-defined patients with PSC using data collected from 3 large-volume, tertiary care centers in Germany and Norway. We analyzed data from 638 patients (70% men; 5900 patient-years of follow-up evaluation); 91 patients had received azathioprine therapy (considered to be effective at 90 days after first intake). Risk analysis was performed using the Cox proportional hazard model when risks competing with study end points were present.
Of patients who received azathioprine treatment, 3.3% developed CCA, compared with 6.8% of patients without azathioprine treatment. However, azathioprine did not significantly affect the risk for CCA (hazard ratio, 0.96; 95% confidence interval, 0.29-3.13; P = .94). The only factor associated with an increased risk of CCA was age 35 years or older at PSC diagnosis (hazard ratio, 3.87; 95% confidence interval, 1.96-7.67; P
PubMed ID
27521513 View in PubMed
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Three ulcerative colitis susceptibility loci are associated with primary sclerosing cholangitis and indicate a role for IL2, REL, and CARD9.

https://arctichealth.org/en/permalink/ahliterature135983
Source
Hepatology. 2011 Jun;53(6):1977-85
Publication Type
Article
Date
Jun-2011
Author
Marcel Janse
Laetitia E Lamberts
Lude Franke
Soumya Raychaudhuri
Eva Ellinghaus
Kirsten Muri Boberg
Espen Melum
Trine Folseraas
Erik Schrumpf
Annika Bergquist
Einar Björnsson
Jingyuan Fu
Harm Jan Westra
Harry J M Groen
Rudolf S N Fehrmann
Joanna Smolonska
Leonard H van den Berg
Roel A Ophoff
Robert J Porte
Tobias J Weismüller
Jochen Wedemeyer
Christoph Schramm
Martina Sterneck
Rainer Günther
Felix Braun
Severine Vermeire
Liesbet Henckaerts
Cisca Wijmenga
Cyriel Y Ponsioen
Stefan Schreiber
Tom H Karlsen
Andre Franke
Rinse K Weersma
Author Affiliation
Department of Gastroenterology and Hepatology, University Medical Center Groningen and University of Groningen, Groningen, The Netherlands.
Source
Hepatology. 2011 Jun;53(6):1977-85
Date
Jun-2011
Language
English
Publication Type
Article
Keywords
Alleles
CARD Signaling Adaptor Proteins - genetics - physiology
Case-Control Studies
Cholangitis, Sclerosing - ethnology - genetics
Cohort Studies
Colitis, Ulcerative - ethnology - genetics
Genetic Predisposition to Disease - ethnology - genetics
Genotype
Germany
Humans
Interleukin-2 - genetics - physiology
Netherlands
Polymorphism, Single Nucleotide - genetics
Proto-Oncogene Proteins c-rel - genetics - physiology
Quantitative Trait Loci
Scandinavia
Abstract
Primary sclerosing cholangitis (PSC) is a chronic cholestatic liver disease characterized by inflammation and fibrosis of the bile ducts. Both environmental and genetic factors contribute to its pathogenesis. To further clarify its genetic background, we investigated susceptibility loci recently identified for ulcerative colitis (UC) in a large cohort of 1,186 PSC patients and 1,748 controls. Single nucleotide polymorphisms (SNPs) tagging 13 UC susceptibility loci were initially genotyped in 854 PSC patients and 1,491 controls from Benelux (331 cases, 735 controls), Germany (265 cases, 368 controls), and Scandinavia (258 cases, 388 controls). Subsequently, a joint analysis was performed with an independent second Scandinavian cohort (332 cases, 257 controls). SNPs at chromosomes 2p16 (P-value 4.12 × 10(-4) ), 4q27 (P-value 4.10 × 10(-5) ), and 9q34 (P-value 8.41 × 10(-4) ) were associated with PSC in the joint analysis after correcting for multiple testing. In PSC patients without inflammatory bowel disease (IBD), SNPs at 4q27 and 9q34 were nominally associated (P
Notes
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PubMed ID
21425313 View in PubMed
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