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  • Vieth, Michael  (16)
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  • 1
    Language: English
    In: Gastroenterology, April 2016, Vol.150(4), pp.S958-S958
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/S0016-5085(16)33236-X Byline: Lothar Veits, Andreas Poetzl, Johannes Schumacher, Nils Kosiol, Jessica Becker, Ines Gockel, Ralf J. Rieker, Michael Vieth
    Keywords: Medicine
    ISSN: 0016-5085
    E-ISSN: 1528-0012
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  • 2
    Language: English
    In: Gastroenterology, April 2017, Vol.152(5), pp.S1028-S1028
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/S0016-5085(17)33478-9 Byline: Marino Venerito, Friederike Weise, Elisabetta Goni, Dirk Reinhold, Karsten Ridwelski, Philipp Lingohr, Hanno Matthaei, Claus Schildberg, Martin Kruschewski, Iurii Krasniuk, Peter P. Grimminger, Markus Moehler, Stefanie Wolff, Hans Lippert, Michael Vieth, Lothar Veits, Christiane Bruns, Florian Lordick, Ines Gockel, Peter Malfertheiner, Johannes Schumacher
    Keywords: Medicine
    ISSN: 0016-5085
    E-ISSN: 1528-0012
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  • 3
    Language: English
    In: Gastric Cancer, 2015, Vol.18(3), pp.550-563
    Description: Byline: Markus Moehler (1,17), Christoph T. H. Baltin (5), Matthias Ebert (2), Wolfgang Fischbach (3), Ines Gockel (1), Lars Grenacher (4), Arnulf H. Holscher (5), Florian Lordick (6), Peter Malfertheiner (7), Helmut Messmann (8), Hans-Joachim Meyer (9), Anne Palmqvist (1), Christoph Rocken (10), Christoph Schuhmacher (11), Michael Stahl (12), Martin Stuschke (13), Michael Vieth (14), Christian Wittekind (15), Dorothea Wagner (16), Stefan P. Monig (5) Keywords: Guidelines; Esophageal cancer; Gastric cancer; Perioperative therapy; Diagnosis Abstract: Background Clinical guidelines are essential in implementing and maintaining nationwide stage-specific diagnostic and therapeutic standards. In 2011, the first German expert consensus guideline defined the evidence for diagnosis and treatment of early and locally advanced esophagogastric cancers. Here, we compare this guideline with other national guidelines as well as current literature. Methods The German S3-guideline used an approved development process with de novo literature research, international guideline adaptation, or good clinical practice. Other recent evidence-based national guidelines and current references were compared with German recommendations. Results In the German S3 and other Western guidelines, adenocarcinomas of the esophagogastric junction (AEG) are classified according to formerly defined AEG I--III subgroups due to the high surgical impact. To stage local disease, computed tomography of the chest and abdomen and endosonography are reinforced. In contrast, laparoscopy is optional for staging. Mucosal cancers (T1a) should be endoscopically resected "en-bloc" to allow complete histological evaluation of lateral and basal margins. For locally advanced cancers of the stomach or esophagogastric junction (a[yen]T3N+), preferred treatment is preoperative and postoperative chemotherapy. Preoperative radiochemotherapy is an evidence-based alternative for large AEG type I--II tumors (a[yen]T3N+). Additionally, some experts recommend treating T2 tumors with a similar approach, mainly because pretherapeutic staging is often considered to be unreliable. Conclusions The German S3 guideline represents an up-to-date European position with regard to diagnosis, staging, and treatment recommendations for patients with locally advanced esophagogastric cancer. Effects of perioperative chemotherapy versus chemoradiotherapy are still to be investigated for adenocarcinoma of the cardia and the lower esophagus. Author Affiliation: (1) University Medical Center Mainz, Mainz, Germany (2) University Medical Center Mannheim, Mannheim, Germany (3) Klinikum Aschaffenburg, Aschaffenburg, Germany (4) Heidelberg University Hospital, Heidelberg, Germany (5) University Hospital of Cologne, Cologne, Germany (6) Klinikum Braunschweig, Braunschweig, Germany (7) University Clinic Magdeburg, Magdeburg, Germany (8) Klinikum Augsburg, Augsburg, Germany (9) Stadtisches Klinikum Solingen, Solingen, Germany (10) Charite Universitatsmedizin Berlin, Berlin, Germany (11) University Hospital Klinikum Rechts der Isar, Munich, Germany (12) Kliniken Essen-Mitte, Essen, Germany (13) Essen University Hospital, Essen, Germany (14) Klinikum Bayreuth, Bayreuth, Germany (15) Universitatsmedizin Leipzig, Leipzig, Germany (16) Center Hospitalier Universitaire Vaudois, Lausanne, Switzerland (17) Medizinische Klinik und Poliklinik, Johannes-Gutenberg-Universitat, Langenbeckstra[sz]e, 155101, Mainz, Germany Article History: Registration Date: 16/07/2014 Received Date: 07/10/2013 Accepted Date: 13/07/2014 Online Date: 07/09/2014 Article note: M. Moehler and C.T.H. Baltin contributed equally. Electronic supplementary material The online version of this article (doi: 10.1007/s10120-014-0403-x) contains supplementary material, which is available to authorized users.
    Keywords: Guidelines ; Esophageal cancer ; Gastric cancer ; Perioperative therapy ; Diagnosis
    ISSN: 1436-3291
    E-ISSN: 1436-3305
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  • 4
    In: European Journal of Human Genetics, 2016
    Description: Idiopathic achalasia is a severe motility disorder of the esophagus and is characterized by a failure of the lower esophageal sphincter to relax due to a loss of neurons in the myenteric plexus. Most recently, we identified an eight-amino-acid insertion in the cytoplasmic tail of HLA-DQβ1 as strong achalasia risk factor in a sample set from Central Europe, Italy and Spain. Here, we tested whether the HLA-DQβ1 insertion also confers achalasia risk in the Polish and Swedish population. We could replicate the initial findings and the insertion shows strong achalasia association in both samples (Poland P=1.84 × 10(-04), Sweden P=7.44 × 10(-05)). Combining all five European data sets - Central Europe, Italy, Spain, Poland and Sweden - the insertion is achalasia associated with Pcombined=1.67 × 10(-35). In addition, we observe that the frequency of the insertion shows a geospatial north-south gradient. The insertion is less common in northern (around 6-7% in patients and 2% in controls from Sweden and Poland) compared with southern Europeans (~16% in patients and 8% in controls from Italy) and shows a stronger attributable risk in the southern European population. Our study provides evidence that the prevalence of achalasia may differ between populations.
    Keywords: Medicine ; Biology;
    ISSN: 1018-4813
    E-ISSN: 14765438
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  • 5
    In: Cancer Medicine, November 2015, Vol.4(11), pp.1700-1704
    Description: The Barrett's and Esophageal Adenocarcinoma Consortium () recently performed a genome‐wide association study () on esophageal adenocarcinoma () and Barrett's esophagus. They identified genome‐wide significant association for variants at three genes, namely ,, and . Furthermore, they replicated an association at the gene that has been previously found in a on Barrett's esophagus. We aimed at further replicating the association at these and other loci that showed suggestive association with  〈  10 in the sample. In total, we tested 88 s in an independent sample consisting of 1065 cases and 1019 controls of German descent. We could replicate the association at ,, and with nominal significance and thereby confirm that genetic variants at these genes confer risk. In addition, we found association of variants near the genes and that were strongly ( 〈 10) although not genome‐wide significantly associated with the . Therefore, both variants and corresponding genes represent promising candidates for future association studies on independent samples. We followed up 88 s which showed association in a genome‐wide association study on esophageal adenocarcinoma (). Our screening sample comprised 1065 cases and 1019 controls. The study provides supportive evidence that s near ,, and confer risk. In addition, we found association at and representing new and promising candidates for future studies on .
    Keywords: Barx 1 ; Esophageal Adenocarcinoma ; Foxf 1 ; Foxp 1 ; Genetic Association Study
    ISSN: 2045-7634
    E-ISSN: 2045-7634
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  • 6
    In: European Journal of Gastroenterology & Hepatology, 2016, Vol.28(6), pp.689-695
    Description: BACKGROUND AND AIM: Although an eight-residue insertion in HLA-DQβ1 has been recently identified as a genetic risk factor for idiopathic achalasia, other risk factors are still unknown. In the present study, we carried out an epidemiological survey and a genotype–phenotype (G×P) analysis to gain further insights into the etiology of achalasia. METHODS: We obtained medical data from 696 achalasia patients and 410 controls, as well as their first-degree relatives (2543 of patients and 1497 of controls). For the G×P analysis, we stratified the patients into HLA-DQβ1 insertion carriers and noncarriers. RESULTS: Our data show that patients are more often affected by viral infections before achalasia onset (P〈0.0001, most significantly for varicella zoster virus infections). In addition, allergic (P=0.0005) and autoimmune disorders (P=0.0007, most significantly for psoriasis and Sjögren’s syndrome) represent comorbid disease conditions. First-degree relatives of patients also show higher prevalence rates of allergic disorders (P=0.0007) and psoriasis (P=0.016) compared with control relatives. Moreover, the G×P analysis reveals that achalasia is triggered by pregnancies in female HLA-DQβ1 insertion carriers (P=0.031). CONCLUSION: Our data point to a role of viral infections in the development of achalasia. In addition, they provide evidence for a relationship between achalasia and allergic, as well as autoimmune, disorders. Furthermore, pregnancy seems to be a disease-triggering factor in female HLA-DQβ1 insertion carriers, which points to hormonal and/or immunosuppressive factors influencing disease development.
    Keywords: Adult–Epidemiology ; Alleles–Epidemiology ; Autoimmune Diseases–Epidemiology ; Case-Control Studies–Genetics ; Chickenpox–Epidemiology ; Comorbidity–Genetics ; Esophageal Achalasia–Genetics ; Europe–Epidemiology ; European Continental Ancestry Group–Epidemiology ; Family–Epidemiology ; Female–Genetics ; Genotype–Epidemiology ; HLA-Dq Beta-Chains–Epidemiology ; Herpes Zoster–Epidemiology ; Herpesvirus 3, Human–Epidemiology ; Heterozygote–Epidemiology ; Humans–Epidemiology ; Hypersensitivity–Epidemiology ; Male–Epidemiology ; Middle Aged–Epidemiology ; Phenotype–Epidemiology ; Pregnancy–Epidemiology ; Pregnancy Complications–Epidemiology ; Psoriasis–Epidemiology ; Sjogren'S Syndrome–Epidemiology ; Virus Diseases–Epidemiology ; HLA-Dq Beta-Chains ; HLA-Dqb1 Antigen;
    ISSN: 0954-691X
    E-ISSN: 14735687
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  • 7
    In: Cancer Medicine, May 2016, Vol.5(5), pp.888-891
    Description: Barrett's esophagus () and esophageal adenocarcinoma () represent two stages within the esophagitis‐metaplasia‐dysplasia‐adenocarcinoma sequence. Previously genetic risk factors have been identified that confer risk to and development. However, to which extent the genetic variants confer risk to different stages of the / sequence remains mainly unknown. In this study we analyzed three most recently identified variants at the genes (rs3072), (rs2701108), and (rs3784262) separately in and samples in order to determine their risk effects during / sequence. Our data show that rs3072 at and rs2701108 at are also associated with and conclude that both loci confer disease risk also at later stages of the / sequence. In contrast, rs3784262 at was highly significantly associated with , but showed no association with . Our data do not provide evidence that the locus confers equal risk in early and late stages of / sequence. The authors followed up SNPs at , and that showed association with Barrett's esophagus (BE) in a previous study. The sample comprised 542 BE and 1106 esophageal adenocarcinoma (EAC) cases as well as 1602 controls. SNPs at and are also associated with EAC and thereby risk‐conferring also to later stages of the BE/EAC sequence. The variant at is associated with BE only, which indicates that this locus plays a more prominent role in early stages of the BE/EAC sequence.
    Keywords: Esophageal Adenocarcinoma ; Genetic Association Study ; Tbx 5 ; Gdf 7 ; Aldh 1a2
    ISSN: 2045-7634
    E-ISSN: 2045-7634
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  • 8
    In: Cancer Medicine, October 2018, Vol.7(10), pp.5057-5065
    Description: Genetic associations between variants on chromosome 5p13 and 8q24 and gastric cancer () have been previously reported in the Asian population. We aimed to replicate these findings and to characterize the associations at the genome and transcriptome level. We performed a fine‐mapping association study in 1926 patients and 2012 controls of European descent using high dense marker sets on both chromosomal regions. Next, we performed expression quantitative trait locus () analyses using gastric transcriptome data from 143 individuals focusing on the associated variants. On chromosome 5p13 the strongest association was observed at rs6872282 ( = 2.53 × 10) and on chromosome 8q24 at rs2585176 ( = 1.09 × 10). On chromosome 5p13 we found cis‐ effects with an upregulation of 4 expression in risk allele carrier ( = 9.27 × 10). On chromosome 8q24 we observed cis‐ effects with an upregulation of expression in risk allele carrier ( = 2.17 × 10). In addition, we found trans‐ effects for the same variants on 8q24 with a downregulation of 7 expression in risk allele carrier ( = 3.11 × 10). In summary, we confirmed and refined the previously reported associations at both chromosomal regions. Our data point to shared etiological factors between Asians and Europeans. Furthermore, our data imply an upregulated expression of 4 and as well as a downregulated expression of 7 in gastric tissue as risk‐conferring pathomechanisms. Genetic variants at chromosome 5p13 and 8q24 contribute to gastric cancer (GC) risk. Expression quantitative trait loci (eQTLs) involving PTGER4 (5p13), PSCA (8q24), and MBOAT7 may act as underlying pathomechanisms.
    Keywords: Eqtl Study ; Gene Expression ; Genetic Association Study ; Stomach Neoplasms
    ISSN: 2045-7634
    E-ISSN: 2045-7634
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  • 9
    Language: English
    In: BMC gastroenterology, 06 March 2019, Vol.19(1), pp.38
    Description: An altered Wnt-signaling activation has been reported during Barrett's esophagus progression, but with rarely detected mutations in APC and β-catenin (CTNNB1) genes. In this study, a robust in-depth expression pattern analysis of frizzled receptors, co-receptors, the Wnt-ligands Wnt3a and Wnt5a, the Wnt-signaling downstream targets Axin2, and CyclinD1, as well as the activation of the intracellular signaling kinases Akt and GSK3β was performed in an in vitro cell culture model of Barrett's esophagus. Representing the Barrett's sequence, we used normal esophageal squamous epithelium (EPC-1, EPC-2), metaplasia (CP-A) and dysplasia (CP-B) to esophageal adenocarcinoma (EAC) cell lines (OE33, OE19) and primary specimens of squamous epithelium, metaplasia and EAC. A loss of Wnt3a expression was observed beginning from the metaplastic cell line CP-A towards dysplasia (CP-B) and EAC (OE33 and OE19), confirmed by a lower staining index of WNT3A in Barrett's metaplasia and EAC, than in squamous epithelium specimens. Frizzled 1-10 expression analysis revealed a distinct expression pattern, showing the highest expression for Fzd2, Fzd3, Fzd4, Fzd5, Fzd7, and the co-receptor LRP5/6 in EAC cells, while Fzd3 and Fzd7 were rarely expressed in primary specimens from squamous epithelium. Despite the absence of an in-depth characterization of Wnt-signaling-associated receptors in Barrett's esophagus, by showing variations of the Fzd- and co-receptor profiles, we provide evidence to have a significant role during Barrett's progression and the underlying pathological mechanisms.
    Keywords: Barrett’s Esophagus ; Esophageal Adenocarcinoma ; Frizzled Receptors ; Wnt-Signaling ; Wnt3a ; Barrett Esophagus -- Genetics ; Wnt Signaling Pathway -- Genetics ; Beta Catenin -- Genetics
    E-ISSN: 1471-230X
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  • 10
    Language: English
    In: The Lancet Oncology, October 2016, Vol.17(10), pp.1363-1373
    Description: Oesophageal adenocarcinoma represents one of the fastest rising cancers in high-income countries. Barrett's oesophagus is the premalignant precursor of oesophageal adenocarcinoma. However, only a few patients with Barrett's oesophagus develop adenocarcinoma, which complicates clinical management in the absence of valid predictors. Within an international consortium investigating the genetics of Barrett's oesophagus and oesophageal adenocarcinoma, we aimed to identify novel genetic risk variants for the development of Barrett's oesophagus and oesophageal adenocarcinoma. We did a meta-analysis of all genome-wide association studies of Barrett's oesophagus and oesophageal adenocarcinoma available in PubMed up to Feb 29, 2016; all patients were of European ancestry and disease was confirmed histopathologically. All participants were from four separate studies within Europe, North America, and Australia and were genotyped on high-density single nucleotide polymorphism (SNP) arrays. Meta-analysis was done with a fixed-effects inverse variance-weighting approach and with a standard genome-wide significance threshold (p〈5 × 10 ). We also did an association analysis after reweighting of loci with an approach that investigates annotation enrichment among genome-wide significant loci. Furthermore, the entire dataset was analysed with bioinformatics approaches—including functional annotation databases and gene-based and pathway-based methods—to identify pathophysiologically relevant cellular mechanisms. Our sample comprised 6167 patients with Barrett's oesophagus and 4112 individuals with oesophageal adenocarcinoma, in addition to 17 159 representative controls from four genome-wide association studies in Europe, North America, and Australia. We identified eight new risk loci associated with either Barrett's oesophagus or oesophageal adenocarcinoma, within or near the genes (rs17451754; p=4·8 × 10 ), (rs17749155; p=5·2 × 10 ), and (rs10108511; p=2·1 × 10 ), (rs62423175; p=3·0 × 10 ), and (rs9918259; p=3·2 × 10 ), (rs7852462; p=1·5 × 10 ), (rs139606545; p=2·0 × 10 ), and and (rs9823696; p=1·6 × 10 ). The locus identified near and (rs9823696) was associated specifically with oesophageal adenocarcinoma (p=1·6 × 10 ) and was independent of Barrett's oesophagus development (p=0·45). A ninth novel risk locus was identified within the gene (rs12207195; posterior probability 0·925) after reweighting with significantly enriched annotations. The strongest disease pathways identified (p〈10 ) belonged to muscle cell differentiation and to mesenchyme development and differentiation. Our meta-analysis of genome-wide association studies doubled the number of known risk loci for Barrett's oesophagus and oesophageal adenocarcinoma and revealed new insights into causes of these diseases. Furthermore, the specific association between oesophageal adenocarcinoma and the locus near and might constitute a novel genetic marker for prediction of the transition from Barrett's oesophagus to oesophageal adenocarcinoma. Fine-mapping and functional studies of new risk loci could lead to identification of key molecules in the development of Barrett's oesophagus and oesophageal adenocarcinoma, which might encourage development of advanced prevention and intervention strategies. US National Cancer Institute, US National Institutes of Health, National Health and Medical Research Council of Australia, Swedish Cancer Society, Medical Research Council UK, Cambridge NIHR Biomedical Research Centre, Cambridge Experimental Cancer Medicine Centre, Else Kröner Fresenius Stiftung, Wellcome Trust, Cancer Research UK, AstraZeneca UK, University Hospitals of Leicester, University of Oxford, Australian Research Council.
    Keywords: Medicine
    ISSN: 1470-2045
    E-ISSN: 1474-5488
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