% IMPORTANT: The following is UTF-8 encoded. This means that in the presence % of non-ASCII characters, it will not work with BibTeX 0.99 or older. % Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or % “biber”. @ARTICLE{Hess:276194, author = {T. Hess and C. Maj and J. Gehlen and O. Borisov and S. L. Haas and I. Gockel and M. Vieth and G. Piessen and H. Alakus and Y. Vashist and C. Pereira and M. Knapp and V. Schüller and A. Quaas and H. I. Grabsch and J. Trautmann and E. Malecka-Wojciesko and A. Mokrowiecka and J. Speller and A. Mayr and J. Schröder and A. M. Hillmer and D. Heider and F. Lordick and Á. Pérez-Aísa and R. Campo and J. Espinel and F. Geijo and C. Thomson and L. Bujanda and F. Sopeña and Á. Lanas and M. Pellisé and C. Pauligk and T. O. Goetze and C. Zelck and J. Reingruber and E. Hassanin and P. Elbe and S. Alsabeah and M. Lindblad and M. Nilsson and N. Kreuser and R. Thieme and F. Tavano and R. Pastorino and D. Arzani and R. Persiani and J.-O. Jung and H. Nienhüser and K. Ott and R. R. Schumann and O. Kumpf and S. Burock and V. Arndt$^*$ and A. Jakubowska and M. Ławniczak and V. Moreno and V. Martín and M. Kogevinas and M. Pollán and J. Dąbrowska and A. Salas and O. Cussenot and A. Boland-Auge and D. Daian and J.-F. Deleuze and E. Salvi and M. Teder-Laving and G. Tomasello and M. Ratti and C. Senti and V. De Re and A. Steffan and A. H. Hölscher and K. Messerle and C. J. Bruns and A. Sīviņš and I. Bogdanova and J. Skieceviciene and J. Arstikyte and M. Moehler and H. Lang and P. P. Grimminger and M. Kruschewski and N. Vassos and C. Schildberg and P. Lingohr and K. Ridwelski and H. Lippert and N. Fricker and P. Krawitz and P. Hoffmann and M. M. Nöthen and L. Veits and J. R. Izbicki and A. Mostowska and F. Martinón-Torres and D. Cusi and R. Adolfsson and G. Cancel-Tassin and A. Höblinger and E. Rodermann and M. Ludwig and G. Keller and A. Metspalu and H. Brenner$^*$ and J. Heller and M. Neef and M. Schepke and F. L. Dumoulin and L. Hamann and R. Cannizzaro and M. Ghidini and D. Plaßmann and M. Geppert and P. Malfertheiner and O. Gehlen and T. Skoczylas and M. Majewski and J. Lubiński and O. Palmieri and S. Boccia and A. Latiano and N. Aragones and T. Schmidt and M. Dinis-Ribeiro and R. Medeiros and S.-E. Al-Batran and M. Leja and J. Kupcinskas and M. A. García-González and M. Venerito and J. Schumacher}, title = {{D}issecting the genetic heterogeneity of gastric cancer.}, journal = {EBioMedicine}, volume = {92}, issn = {2352-3964}, address = {Amsterdam [u.a.]}, publisher = {Elsevier}, reportid = {DKFZ-2023-01016}, pages = {104616}, year = {2023}, abstract = {Gastric cancer (GC) is clinically heterogenous according to location (cardia/non-cardia) and histopathology (diffuse/intestinal). We aimed to characterize the genetic risk architecture of GC according to its subtypes. Another aim was to examine whether cardia GC and oesophageal adenocarcinoma (OAC) and its precursor lesion Barrett's oesophagus (BO), which are all located at the gastro-oesophageal junction (GOJ), share polygenic risk architecture.We did a meta-analysis of ten European genome-wide association studies (GWAS) of GC and its subtypes. All patients had a histopathologically confirmed diagnosis of gastric adenocarcinoma. For the identification of risk genes among GWAS loci we did a transcriptome-wide association study (TWAS) and expression quantitative trait locus (eQTL) study from gastric corpus and antrum mucosa. To test whether cardia GC and OAC/BO share genetic aetiology we also used a European GWAS sample with OAC/BO.Our GWAS consisting of 5816 patients and 10,999 controls highlights the genetic heterogeneity of GC according to its subtypes. We newly identified two and replicated five GC risk loci, all of them with subtype-specific association. The gastric transcriptome data consisting of 361 corpus and 342 antrum mucosa samples revealed that an upregulated expression of MUC1, ANKRD50, PTGER4, and PSCA are plausible GC-pathomechanisms at four GWAS loci. At another risk locus, we found that the blood-group 0 exerts protective effects for non-cardia and diffuse GC, while blood-group A increases risk for both GC subtypes. Furthermore, our GWAS on cardia GC and OAC/BO (10,279 patients, 16,527 controls) showed that both cancer entities share genetic aetiology at the polygenic level and identified two new risk loci on the single-marker level.Our findings show that the pathophysiology of GC is genetically heterogenous according to location and histopathology. Moreover, our findings point to common molecular mechanisms underlying cardia GC and OAC/BO.German Research Foundation (DFG).}, keywords = {Gastric cancer (Other) / Genome-wide association study (GWAS) (Other) / Oesophageal adenocarcinoma (Other) / Transcriptome-wide association study (TWAS) (Other)}, cin = {C071 / C070 / C120 / HD01}, ddc = {610}, cid = {I:(DE-He78)C071-20160331 / I:(DE-He78)C070-20160331 / I:(DE-He78)C120-20160331 / I:(DE-He78)HD01-20160331}, pnm = {313 - Krebsrisikofaktoren und Prävention (POF4-313)}, pid = {G:(DE-HGF)POF4-313}, typ = {PUB:(DE-HGF)16}, pubmed = {pmid:37209533}, doi = {10.1016/j.ebiom.2023.104616}, url = {https://inrepo02.dkfz.de/record/276194}, }