Schildhaus, Hans-Ulrich

[["dc.bibliographiccitation.firstpage","10577"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","10585"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Scheffler, Matthias"],["dc.contributor.author","Schultheis, Anne"],["dc.contributor.author","Teixido, Cristina"],["dc.contributor.author","Michels, Sebastian"],["dc.contributor.author","Morales-Espinosa, Daniela"],["dc.contributor.author","Viteri, Santiago"],["dc.contributor.author","Hartmann, Wolfgang"],["dc.contributor.author","Merkelbach-Bruse, Sabine"],["dc.contributor.author","Fischer, Rieke"],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.contributor.author","Fassunke, Jana"],["dc.contributor.author","Sebastian, Martin"],["dc.contributor.author","Serke, Monika"],["dc.contributor.author","Kaminsky, Britta"],["dc.contributor.author","Randerath, Winfried"],["dc.contributor.author","Gerigk, Ulrich"],["dc.contributor.author","Ko, Yon-Dschun"],["dc.contributor.author","Krüger, Stefan"],["dc.contributor.author","Schnell, Roland"],["dc.contributor.author","Rothe, Achim"],["dc.contributor.author","Kropf-Sanchen, Cornelia"],["dc.contributor.author","Heukamp, Lukas"],["dc.contributor.author","Rosell, Rafael"],["dc.contributor.author","Büttner, Reinhard"],["dc.contributor.author","Wolf, Jürgen"],["dc.date.accessioned","2019-07-09T11:42:39Z"],["dc.date.available","2019-07-09T11:42:39Z"],["dc.date.issued","2015-04-30"],["dc.description.abstract","BACKGROUND: While recent data show that crizotinib is highly effective in patients with ROS1 rearrangement, few data is available about the prognostic impact, the predictive value for different treatments, and the genetic heterogeneity of ROS1-positive patients. PATIENTS AND METHODS: 1137 patients with adenocarcinoma of the lung were analyzed regarding their ROS1 status. In positive cases, next-generation sequencing (NGS) was performed. Clinical characteristics, treatments and outcome of these patients were assessed. Overall survival (OS) was compared with genetically defined subgroups of ROS1-negative patients. RESULTS: 19 patients of 1035 evaluable (1.8%) had ROS1-rearrangement. The median OS has not been reached. Stage IV patients with ROS1-rearrangement had the best OS of all subgroups (36.7 months, p < 0.001). 9 of 14 (64.2%) patients had at least one response to chemotherapy. Estimated mean OS for patients receiving chemotherapy and crizotinib was 5.3 years. Ten patients with ROS1-rearrangement (52.6%) harbored additional aberrations. CONCLUSION: ROS1-rearangement is not only a predictive marker for response to crizotinib, but also seems to be the one of the best prognostic molecular markers in NSCLC reported so far. In stage IV patients, response to chemotherapy was remarkable high and overall survival was significantly better compared to other subgroups including EGFR-mutated and ALK-fusion-positive NSCLC."],["dc.identifier.doi","10.18632/oncotarget.3387"],["dc.identifier.fs","611826"],["dc.identifier.pmid","25868855"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13617"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58716"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1949-2553"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.mesh","Adenocarcinoma"],["dc.subject.mesh","Adult"],["dc.subject.mesh","Aged"],["dc.subject.mesh","Female"],["dc.subject.mesh","Gene Rearrangement"],["dc.subject.mesh","Genetic Variation"],["dc.subject.mesh","Humans"],["dc.subject.mesh","Lung Neoplasms"],["dc.subject.mesh","Male"],["dc.subject.mesh","Middle Aged"],["dc.subject.mesh","Prognosis"],["dc.subject.mesh","Protein-Tyrosine Kinases"],["dc.subject.mesh","Proto-Oncogene Proteins"],["dc.subject.mesh","Survival Analysis"],["dc.subject.mesh","Treatment Outcome"],["dc.title","ROS1 rearrangements in lung adenocarcinoma: prognostic impact, therapeutic options and genetic variability."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["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"]]