Schildhaus, Hans-Ulrich

[["dc.bibliographiccitation.firstpage","20215"],["dc.bibliographiccitation.issue","24"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","20130"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Künstlinger, Helen"],["dc.contributor.author","Fassunke, Jana"],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.contributor.author","Brors, Benedikt"],["dc.contributor.author","Heydt, Carina"],["dc.contributor.author","Ihle, Michaela Angelika"],["dc.contributor.author","Mechtersheimer, Gunhild"],["dc.contributor.author","Wardelmann, Eva"],["dc.contributor.author","Büttner, Reinhard"],["dc.contributor.author","Merkelbach-Bruse, Sabine"],["dc.date.accessioned","2019-07-09T11:42:38Z"],["dc.date.available","2019-07-09T11:42:38Z"],["dc.date.issued","2015-08-21"],["dc.description.abstract","Myxoid liposarcomas account for more than one third of liposarcomas and about 10% of all adult soft tissue sarcomas. The tumors are characterized by specific chromosomal translocations leading to the chimeric oncogenes FUS-DDIT3 or EWS1R-DDIT3. The encoded fusion proteins act as aberrant transcription factors. Therefore, we implemented comparative expression analyses using whole-genome microarrays in tumor and fat tissue samples. We aimed at identifying differentially expressed genes which may serve as diagnostic or prognostic biomarkers or as therapeutic targets. Microarray analyses revealed overexpression of FGFR2 and other members of the FGF/FGFR family. Overexpression of FGFR2 was validated by qPCR, immunohistochemistry and western blot analysis in primary tumor samples. Treatment of the myxoid liposarcoma cell lines MLS 402 and MLS 1765 with the FGFR inhibitors PD173074, TKI258 (dovitinib) and BGJ398 as well as specific siRNAs reduced cell proliferation, induced apoptosis and delayed cell migration. Combination of FGFR inhibitors with trabectedin further increased the effect. Our study demonstrates overexpression of FGFR2 and a functional role of FGFR signaling in myxoid liposarcoma. As FGFR inhibition showed effects on proliferation and cell migration and induced apoptosis in vitro, our data indicate the potential use of FGFR inhibitors as a targeted therapy for these tumors."],["dc.identifier.doi","10.18632/oncotarget.4046"],["dc.identifier.fs","617613"],["dc.identifier.pmid","26036639"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13611"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58712"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1949-2553"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.subject.mesh","Cell Line, Tumor"],["dc.subject.mesh","Cell Movement"],["dc.subject.mesh","Cell Proliferation"],["dc.subject.mesh","Cohort Studies"],["dc.subject.mesh","Gene Expression"],["dc.subject.mesh","Humans"],["dc.subject.mesh","Liposarcoma, Myxoid"],["dc.subject.mesh","Microarray Analysis"],["dc.subject.mesh","Pyrimidines"],["dc.subject.mesh","Receptor, Fibroblast Growth Factor, Type 2"],["dc.subject.mesh","Receptors, Fibroblast Growth Factor"],["dc.subject.mesh","Signal Transduction"],["dc.title","FGFR2 is overexpressed in myxoid liposarcoma and inhibition of FGFR signaling impairs tumor growth in vitro."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","6105"],["dc.bibliographiccitation.issue","23"],["dc.bibliographiccitation.journal","Clinical Cancer Research"],["dc.bibliographiccitation.lastpage","6116"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Wozniak, Agnieszka"],["dc.contributor.author","Rutkowski, Piotr"],["dc.contributor.author","Schoffski, Patrick"],["dc.contributor.author","Ray-Coquard, Isabelle"],["dc.contributor.author","Hostein, Isabelle"],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.contributor.author","Le Cesne, Axel"],["dc.contributor.author","Bylina, Elzbieta"],["dc.contributor.author","Limon, Janusz"],["dc.contributor.author","Blay, Jean-Yves"],["dc.contributor.author","Siedlecki, Janusz A."],["dc.contributor.author","Wardelmann, Eva"],["dc.contributor.author","Sciot, Raf"],["dc.contributor.author","Coindre, Jean-Michel"],["dc.contributor.author","Debiec-Rychter, Maria"],["dc.date.accessioned","2018-11-07T09:31:58Z"],["dc.date.available","2018-11-07T09:31:58Z"],["dc.date.issued","2014"],["dc.description.abstract","Purpose: Although the mutational status in gastrointestinal stromal tumors (GIST) can predict the response to treatment with tyrosine kinase inhibitors, the role of tumor genotype as a prognostic factor remains controversial. The ConticaGIST study sought to determine the pathologic and molecular factors associated with disease-free survival (DFS) in patients with operable, imatinib-naive GIST. Experimental Design: Clinicopathologic and molecular data from 1,056 patients with localized GIST who underwent surgery with curative intention (R0/R1) and were registered in the European ConticaGIST database were prospectively obtained and reviewed. Risk of tumor recurrence was stratified using the modified NIH criteria. The median follow-up was 52 months. Results: On testing for potential prognostic parameters, the following were associated with inferior DFS on multivariable Cox model analysis: primary nongastric site, size > 10 cm, mitotic index > 10 mitoses per 50 high power field, and the KIT exon 9 duplication [hazard ratio (HR), 1.47; 95% confidence interval (CI), 0.9-2.5; P = 0.037] and KIT exon 11 deletions involving codons 557 and/or 558 [KITdel-inc557/558; HR, 1.45; 95% CI, 1.0-2.2; P = 0.004]. Conversely, PDGFRA exon 18 mutations were indicators of better prognosis [HR, 0.23; 95% CI, 0.1-0.6; P = 0.002]. KITdel-inc557/558 were an adverse indicator only in GIST localized in the stomach (P < 0.001) but not in tumors with nongastric origin. In gastric GIST, all other mutations presented remarkably superior 5-year DFS. Conclusions: In conclusion, tumor genotype is an independent molecular prognostic variable associated with gastric GIST and should be used for optimizing tailored adjuvant imatinib treatment. (C) 2014 AACR."],["dc.identifier.doi","10.1158/1078-0432.CCR-14-1677"],["dc.identifier.isi","000346417400027"],["dc.identifier.pmid","25294914"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31643"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Cancer Research"],["dc.relation.issn","1557-3265"],["dc.relation.issn","1078-0432"],["dc.title","Tumor Genotype Is an Independent Prognostic Factor in Primary Gastrointestinal Stromal Tumors of Gastric Origin: A European Multicenter Analysis Based on ConticaGIST"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Modern Pathology"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Schildhaus, H-U"],["dc.contributor.author","Binot, Elke"],["dc.contributor.author","Buttner, R."],["dc.contributor.author","Tancheva-Poor, I."],["dc.contributor.author","Wardelmann, Eva"],["dc.date.accessioned","2018-11-07T09:44:20Z"],["dc.date.available","2018-11-07T09:44:20Z"],["dc.date.issued","2014"],["dc.format.extent","28A"],["dc.identifier.isi","000331502200099"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34370"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.publisher.place","New york"],["dc.relation.conference","103rd Annual Meeting of the United-States-and-Canadian-Academy-of-Pathology (USCAP)"],["dc.relation.eventlocation","San Diego, CA"],["dc.relation.issn","1530-0285"],["dc.relation.issn","0893-3952"],["dc.title","Validation of Break Apart FISH Probes for the Detection of COL1A1-PDGFB Rearrangements in Dermatofibrosarcoma Protuberans"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Laboratory Investigation"],["dc.bibliographiccitation.volume","94"],["dc.contributor.author","Schildhaus, H-U"],["dc.contributor.author","Binot, Elke"],["dc.contributor.author","Buttner, R."],["dc.contributor.author","Tancheva-Poor, I."],["dc.contributor.author","Wardelmann, Eva"],["dc.date.accessioned","2018-11-07T09:44:19Z"],["dc.date.available","2018-11-07T09:44:19Z"],["dc.date.issued","2014"],["dc.format.extent","28A"],["dc.identifier.isi","000331155800099"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34365"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.publisher.place","New york"],["dc.relation.conference","103rd Annual Meeting of the United-States-and-Canadian-Academy-of-Pathology (USCAP)"],["dc.relation.eventlocation","San Diego, CA"],["dc.relation.issn","1530-0307"],["dc.relation.issn","0023-6837"],["dc.title","Validation of Break Apart FISH Probes for the Detection of COL1A1-PDGFB Rearrangements in Dermatofibrosarcoma Protuberans"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","206"],["dc.bibliographiccitation.journal","Human Pathology"],["dc.bibliographiccitation.lastpage","214"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Huss, Sebastian"],["dc.contributor.author","Pasternack, Helen"],["dc.contributor.author","Ihle, Michaela Angelika"],["dc.contributor.author","Merkelbach-Bruse, Sabine"],["dc.contributor.author","Heitkoetter, Birthe"],["dc.contributor.author","Hartmann, Wolfgang"],["dc.contributor.author","Trautmann, Marcel"],["dc.contributor.author","Gevensleben, Heidrun"],["dc.contributor.author","Buettner, Reinhard"],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.contributor.author","Wardelmann, Eva"],["dc.date.accessioned","2018-11-07T10:25:18Z"],["dc.date.available","2018-11-07T10:25:18Z"],["dc.date.issued","2017"],["dc.description.abstract","In KIT/PDGFRA wild-type gastrointestinal stromal tumors (wt-GISTs), BRAF mutations are regarded as alternative pathogenic events driving tumorigenesis. In our study, we aimed at analyzing a large cohort (n = 444) of GISTs for BRAF mutations using molecular and immunohistochemical methods. More than 3000 GIST samples from caucasian patients were available in our GIST and Sarcoma Registry NRW. Of these, we selected 172 wt-GISTs to evaluate the frequency of BRAF mutations. Furthermore, 272 GISTs with a representative KIT and PDGFRA mutational status were selected. BRAF mutational status was evaluated by high-resolution melting analysis, Sanger sequencing, and VE1 immunohistochemistry. A BRAF mutation (p.V600E) was found in 7 cases (3.9%) of the wt-GIST cohort. In 2 cases, multiple synchronous tumors harbored the same somatic BRAF mutation. VE1 immunohistochemical staining had a sensitivity of 81.8% and a specificity of 97.5% to detect BRAF p.V600E mutations. Analyzing our cases and the cases reported in the literature (n = 37), the percentage of intermediate and high-risk BRAF-mutated wt-GISTs (17/31; 54.8%) was comparable to that recorded for large GIST cohorts irrespective of the mutational status. BRAF mutations are rare events in wt-GISTs, and VE1 immunohistochemistry appears to be a valuable pre-screening tool for the detection of BRAF p.V600E mutations. BRAF mutations in GISTs do not seem to have a prognostic value per se. However, as BRAF inhibition represents a therapeutic option to control disease, we suggest the assessment of the BRAF mutational status, especially in the setting of advanced GIST disease. (C) 2017 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.humpath.2017.01.005"],["dc.identifier.isi","000400230800027"],["dc.identifier.pmid","28159677"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42831"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","W B Saunders Co-elsevier Inc"],["dc.relation.issn","1532-8392"],["dc.relation.issn","0046-8177"],["dc.title","Clinicopathological and molecular features of a large cohort of gastrointestinal stromal tumors (GISTs) and review of the literature: BRAF mutations in KIT/PDGFRA wild-type GISTs are rare events"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e0193048"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","PLoS One"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Ihle, Michaela Angelika"],["dc.contributor.author","Huss, Sebastian"],["dc.contributor.author","Jeske, Wiebke"],["dc.contributor.author","Hartmann, Wolfgang"],["dc.contributor.author","Merkelbach-Bruse, Sabine"],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.contributor.author","Büttner, Reinhard"],["dc.contributor.author","Sihto, Harri"],["dc.contributor.author","Sundby Hall, Kirsten"],["dc.contributor.author","Eriksson, Mikael"],["dc.contributor.author","Reichardt, Peter"],["dc.contributor.author","Joensuu, Heikki"],["dc.contributor.author","Wardelmann, Eva"],["dc.contributor.editor","Duensing, Anette"],["dc.date.accessioned","2020-12-10T18:42:06Z"],["dc.date.available","2020-12-10T18:42:06Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1371/journal.pone.0193048"],["dc.identifier.eissn","1932-6203"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15678"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77804"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Expression of cell cycle regulators and frequency of TP53 mutations in high risk gastrointestinal stromal tumors prior to adjuvant imatinib treatment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","59"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","The Journal of Pathology"],["dc.bibliographiccitation.lastpage","71"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Angelika Ihle, Michaela"],["dc.contributor.author","Merkelbach‐Bruse, Sabine"],["dc.contributor.author","Hartmann, Wolfgang"],["dc.contributor.author","Bauer, Sebastian"],["dc.contributor.author","Ratner, Nancy"],["dc.contributor.author","Sonobe, Hiroshi"],["dc.contributor.author","Nishio, Jun"],["dc.contributor.author","Larsson, Olle"],["dc.contributor.author","Åman, Pierre"],["dc.contributor.author","Pedeutour, Florence"],["dc.contributor.author","Taguchi, Takahiro"],["dc.contributor.author","Wardelmann, Eva"],["dc.contributor.author","Buettner, Reinhard"],["dc.contributor.author","Schildhaus, Hans‐Ulrich"],["dc.date.accessioned","2020-12-10T14:05:57Z"],["dc.date.available","2020-12-10T14:05:57Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.1002/cjp2.v2.2"],["dc.identifier.eissn","2056-4538"],["dc.identifier.issn","2056-4538"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/69719"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","HR23b expression is a potential predictive biomarker for HDAC inhibitor treatment in mesenchymal tumours and is associated with response to vorinostat"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","106"],["dc.bibliographiccitation.journal","BMC Medical Genetics"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Merkelbach-Bruse, Sabine"],["dc.contributor.author","Dietmaier, Wolfgang"],["dc.contributor.author","Fuezesi, Laszlo"],["dc.contributor.author","Gaumann, Andreas"],["dc.contributor.author","Haller, Florian"],["dc.contributor.author","Kitz, Julia"],["dc.contributor.author","Krohn, Antje"],["dc.contributor.author","Mechtersheimer, Gunhild"],["dc.contributor.author","Penzel, Roland"],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.contributor.author","Schneider-Stock, Regine"],["dc.contributor.author","Simon, Ronald"],["dc.contributor.author","Wardelmann, Eva"],["dc.date.accessioned","2018-11-07T08:41:25Z"],["dc.date.available","2018-11-07T08:41:25Z"],["dc.date.issued","2010"],["dc.description.abstract","Background: Mutation analysis of KIT and PDGFRA genes in gastrointestinal stromal tumors is gaining increasing importance for prognosis of GISTs and for prediction of treatment response. Several groups have identified specific mutational subtypes in KIT exon 11 associated with an increased risk of metastatic disease whereas GISTs with PDGFRA mutations often behave less aggressive. Furthermore, in advanced GIST disease with proven KIT exon 9 mutation the doubled daily dose of 800 mg imatinib increases the progression free survival and is now recommended both in the European and the American Guidelines. In Germany, there are still no general rules how to perform mutational analysis. Methods: When comparing results from six different molecular laboratories we recognized the need of standardisation. Six German university laboratories with experience in mutation analysis in GISTs joined together to develop recommendations for the mutation analysis of the most common and clinically relevant hot spots, i.e. KIT exons 9 and 11 and PDGFRA exon 18. We performed a three-phased interlaboratory trial to identify pitfalls in performing molecular analysis in GISTs. Results: We developed a design for a continuous external laboratory trial. In 2009 this external trial was conducted by 19 laboratories via the initiative for quality assurance in pathology (QuiP) of the German Society of Pathology and the Professional Association of German Pathologists. Conclusions: By performing a three-phased internal interlaboratory trial and conducting an external trial in Germany we were able to identify potential pitfalls when performing KIT and PDGFRA mutational analysis in gastrointestinal stromal tumors. We developed standard operation procedures which are provided with the manuscript to allow other laboratories to prevent these pitfalls."],["dc.description.sponsorship","Novartis"],["dc.identifier.doi","10.1186/1471-2350-11-106"],["dc.identifier.isi","000280824500001"],["dc.identifier.pmid","20598160"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5671"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19467"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1471-2350"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Pitfall in mutational testing and reporting of common KIT and PDGFRA mutations in gastrointestinal stromal tumors"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","UNSP e0120079"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Schmitz, Katja"],["dc.contributor.author","Koeppen, Hartmut"],["dc.contributor.author","Binot, Elke"],["dc.contributor.author","Fassunke, Jana"],["dc.contributor.author","Kuenstlinger, Helen"],["dc.contributor.author","Ihle, Michaela Angelika"],["dc.contributor.author","Heydt, Carina"],["dc.contributor.author","Wardelmann, Eva"],["dc.contributor.author","Buettner, Reinhard"],["dc.contributor.author","Merkelbach-Bruse, Sabine"],["dc.contributor.author","Rueschoff, Josef"],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.date.accessioned","2018-11-07T09:58:38Z"],["dc.date.available","2018-11-07T09:58:38Z"],["dc.date.issued","2015"],["dc.description.abstract","Soft tissue sarcomas are a heterogeneous group of tumors with many different subtypes. In 2014 an estimated 12,020 newly diagnosed cases and 4,740 soft tissue sarcoma related deaths can be expected in the United States. Many soft tissue sarcomas are associated with poor prognosis and therapeutic options are often limited. The evolution of precision medicine has not yet fully reached the clinical treatment of sarcomas since therapeutically tractable genetic changes have not been comprehensively studied so far. We analyzed a total of 484 adult-type malignant mesenchymal tumors by MET fluorescence in situ hybridization and MET and hepatocyte growth factor immunohistochemistry. Eleven different entities were included, among them the most common and clinically relevant subtypes and tumors with specific translocations or complex genetic changes. MET protein expression was observed in 2.6% of the cases, all of which were either undifferentiated pleomorphic sarcomas or angiosarcomas, showing positivity rates of 14% and 17%, respectively. 6% of the tumors showed hepatocyte growth factor overexpression, mainly seen in undifferentiated pleomorphic sarcomas and angiosarcomas, but also in clear cell sarcomas, malignant peripheral nerve sheath tumors, leiomyosarcomas and gastrointestinal stromal tumors. MET and hepatocyte growth factor overexpression were significantly correlated and may suggest an autocrine activation in these tumors. MET FISH amplification and copy number gain were present in 4% of the tumors (15/413). Two samples, both undifferentiated pleomorphic sarcomas, fulfilled the criteria for high level amplification of MET, one undifferentiated pleomorphic sarcoma reached an intermediate level copy number gain, and 12 samples of different subtypes were categorized as low level copy number gains for MET. Our findings indicate that angiosarcomas and undifferentiated pleomorphic sarcomas rather than other frequent adult-type sarcomas should be enrolled in screening programs for clinical trials with MET inhibitors. The screening methods should include both in situ hybridization and immunohistochemistry."],["dc.description.sponsorship","German Cancer Aid (Deutsche Krebshilfe)"],["dc.identifier.doi","10.1371/journal.pone.0120079"],["dc.identifier.isi","000352475700002"],["dc.identifier.pmid","25844809"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11760"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37407"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","MET Gene Copy Number Alterations and Expression of MET and Hepatocyte Growth Factor Are Potential Biomarkers in Angiosarcomas and Undifferentiated Pleomorphic Sarcomas"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1985"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Molecular Cancer Therapeutics"],["dc.bibliographiccitation.lastpage","1996"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Mühlenberg, Thomas"],["dc.contributor.author","Ketzer, Julia"],["dc.contributor.author","Heinrich, Michael C."],["dc.contributor.author","Grunewald, Susanne"],["dc.contributor.author","Marino-Enriquez, Adrian"],["dc.contributor.author","Trautmann, Marcel"],["dc.contributor.author","Hartmann, Wolfgang"],["dc.contributor.author","Wardelmann, Eva"],["dc.contributor.author","Treckmann, Jürgen"],["dc.contributor.author","Worm, Karl"],["dc.contributor.author","Bertram, Stefanie"],["dc.contributor.author","Herold, Thomas"],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.contributor.author","Glimm, Hanno"],["dc.contributor.author","Stenzinger, Albrecht"],["dc.contributor.author","Brors, Benedikt"],["dc.contributor.author","Horak, Peter"],["dc.contributor.author","Hohenberger, Peter"],["dc.contributor.author","Fröhling, Stefan"],["dc.contributor.author","Fletcher, Jonathan A."],["dc.contributor.author","Bauer, Sebastian"],["dc.date.accessioned","2020-12-10T18:37:47Z"],["dc.date.available","2020-12-10T18:37:47Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1158/1535-7163.MCT-18-1224"],["dc.identifier.eissn","1538-8514"],["dc.identifier.issn","1535-7163"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77089"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","KIT-Dependent and KIT-Independent Genomic Heterogeneity of Resistance in Gastrointestinal Stromal Tumors — TORC1/2 Inhibition as Salvage Strategy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]