Schildhaus, Hans-Ulrich

[["dc.bibliographiccitation.journal","Oncology Research and Treatment"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Scheffler, M."],["dc.contributor.author","Schultheis, A."],["dc.contributor.author","Michels, Sebastian"],["dc.contributor.author","Teixido, Cristina"],["dc.contributor.author","Hartmann, Wolfgang"],["dc.contributor.author","Merkelbach-Bruse, Sabine"],["dc.contributor.author","Sebastian, Martin"],["dc.contributor.author","Serke, Monika Heidi"],["dc.contributor.author","Kropf-Sanchen, Cornelia"],["dc.contributor.author","Wittersheim, M."],["dc.contributor.author","Puetz, K."],["dc.contributor.author","Binot, Elke"],["dc.contributor.author","Schildhaus, H.-U."],["dc.contributor.author","Heukamp, Lukas Carl"],["dc.contributor.author","Rosell, Rafael"],["dc.contributor.author","Buettner, Reinhardt"],["dc.contributor.author","Wolf, J."],["dc.date.accessioned","2018-11-07T09:34:02Z"],["dc.date.available","2018-11-07T09:34:02Z"],["dc.date.issued","2014"],["dc.format.extent","66"],["dc.identifier.isi","000343816900151"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32093"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.publisher.place","Basel"],["dc.relation.issn","2296-5262"],["dc.relation.issn","2296-5270"],["dc.title","ROS1 rearrangement in non-small cell lung cancer (NSCLC): Prognostic and predicitve impact and genetic variability"],["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","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.firstpage","122"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Thoracic Oncology"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Michels, Sebastian"],["dc.contributor.author","Scheel, Andreas Hans Joachim"],["dc.contributor.author","Scheffler, Matthias"],["dc.contributor.author","Schultheis, Anne Maria"],["dc.contributor.author","Gautschi, Oliver Pascal"],["dc.contributor.author","Aebersold, Franziska"],["dc.contributor.author","Diebold, Joachim"],["dc.contributor.author","Pall, Georg"],["dc.contributor.author","Rothschild, Sacha"],["dc.contributor.author","Bubendorf, Lukas"],["dc.contributor.author","Hartmann, Wolfgang"],["dc.contributor.author","Heukamp, Lukas Carl"],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.contributor.author","Fassunke, Jana"],["dc.contributor.author","Ihle, Michaela Angelika"],["dc.contributor.author","Kuenstlinger, Helen"],["dc.contributor.author","Heydt, Carina"],["dc.contributor.author","Fischer, Rieke N."],["dc.contributor.author","Nogova, Lucia"],["dc.contributor.author","Mattonet, Christian"],["dc.contributor.author","Hein, Rebecca"],["dc.contributor.author","Adams, Anne"],["dc.contributor.author","Gerigk, Ulrich"],["dc.contributor.author","Schulte, Wolfgang"],["dc.contributor.author","Lueders, Heike"],["dc.contributor.author","Grohe, Christian"],["dc.contributor.author","Graeven, Ullrich"],["dc.contributor.author","Mueller-Naendrup, Clemens"],["dc.contributor.author","Draube, Andreas"],["dc.contributor.author","Kambartel, Karl-Otto"],["dc.contributor.author","Krüger, Stefan"],["dc.contributor.author","Schulze-Olden, Susanne"],["dc.contributor.author","Serke, Monika"],["dc.contributor.author","Engel-Riedel, Walburga"],["dc.contributor.author","Kaminsky, Britta"],["dc.contributor.author","Randerath, Winfried J."],["dc.contributor.author","Merkelbach-Bruse, Sabine"],["dc.contributor.author","Buettner, Reinhard"],["dc.contributor.author","Wolf, Juergen"],["dc.date.accessioned","2018-11-07T10:20:42Z"],["dc.date.available","2018-11-07T10:20:42Z"],["dc.date.issued","2016"],["dc.description.abstract","Introduction: Rearrangements of RET are rare oncogenic events in patients with non-small cell lung cancer (NSCLC). While the characterization of Asian patients suggests a predominance of nonsmokers of young age in this genetically defined lung cancer subgroup, little is known about the characteristics of non-Asian patients. We present the results of an analysis of a European cohort of patients with RET rearranged NSCLC. Methods: Nine hundred ninety-seven patients with KRAS/EGFR/ALK wildtype lung adenocarcinomas were analyzed using fluorescence in situ hybridization for RET fusions. Tumor specimens were molecularly profiled and clinicopathological characteristics of the patients were collected. Results: Rearrangements of RET were identified in 22 patients, with a prevalence of 2.2% in the KRAS/EGFR/ALK wildtype subgroup. Co-occurring genetic aberrations were detected in 10 patients, and the majority had mutations in TP53. The median age at diagnosis was 62 years (range, 39-80 years; mean +/- SD, 61 +/- 11.7 years) with a higher proportion of men (59% versus 41%). There was only a slight predominance of nonsmokers (54.5%) compared to current or former smokers (45.5%). Conclusions: Patients with RET rearranged adenocarcinomas represent a rare and heterogeneous NSCLC sub-group. In some contrast to published data, we see a high prevalence of current and former smokers in our white RET cohort. The significance of co-occurring aberrations, so far, is unclear. (C) 2015 International Association for the Study of Lung Cancer. Published by Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.jtho.2015.09.016"],["dc.identifier.isi","000373094200014"],["dc.identifier.pmid","26762747"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41941"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","1556-1380"],["dc.relation.issn","1556-0864"],["dc.title","Clinicopathological Characteristics of RET Rearranged Lung Cancer in European Patients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1216"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","1216"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Kemper, Marcel"],["dc.contributor.author","Evers, Georg"],["dc.contributor.author","Schulze, Arik Bernard"],["dc.contributor.author","Sperveslage, Jan"],["dc.contributor.author","Schülke, Christoph"],["dc.contributor.author","Lenz, Georg"],["dc.contributor.author","Herold, Thomas"],["dc.contributor.author","Hartmann, Wolfgang"],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.contributor.author","Bleckmann, Annalen"],["dc.date.accessioned","2022-12-01T08:31:29Z"],["dc.date.available","2022-12-01T08:31:29Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.18632/oncotarget.28293"],["dc.identifier.pii","28293"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/118179"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-621"],["dc.relation.eissn","1949-2553"],["dc.title","Addendum: Polyclonal on- and off-target resistance mutations in an EML4-ALK positive non-small cell lung cancer patient under ALK inhibition"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1946"],["dc.bibliographiccitation.issue","19"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","1952"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Kemper, Marcel"],["dc.contributor.author","Evers, Georg"],["dc.contributor.author","Schulze, Arik Bernard"],["dc.contributor.author","Sperveslage, Jan"],["dc.contributor.author","Schülke, Christoph"],["dc.contributor.author","Lenz, Georg"],["dc.contributor.author","Herold, Thomas"],["dc.contributor.author","Hartmann, Wolfgang"],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.contributor.author","Bleckmann, Annalen"],["dc.date.accessioned","2021-10-01T09:58:40Z"],["dc.date.available","2021-10-01T09:58:40Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.18632/oncotarget.28062"],["dc.identifier.pii","28062"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/90116"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-469"],["dc.relation.eissn","1949-2553"],["dc.title","Polyclonal on- and off-target resistance mutations in an EML4-ALK positive non-small cell lung cancer patient under ALK inhibition"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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"]]

[["dc.bibliographiccitation.firstpage","2578"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","International Journal of Cancer"],["dc.bibliographiccitation.lastpage","2588"],["dc.bibliographiccitation.volume","137"],["dc.contributor.author","Sievers, Elisabeth"],["dc.contributor.author","Trautmann, Marcel"],["dc.contributor.author","Kindler, Dagmar"],["dc.contributor.author","Huss, Sebastian"],["dc.contributor.author","Gruenewald, Inga"],["dc.contributor.author","Dirksen, Uta"],["dc.contributor.author","Renner, Marcus"],["dc.contributor.author","Mechtersheimer, Gunhild"],["dc.contributor.author","Pedeutour, Florence"],["dc.contributor.author","Aman, Pierre"],["dc.contributor.author","Nishio, Jun"],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.contributor.author","Kirfel, Jutta"],["dc.contributor.author","Schirmacher, Peter"],["dc.contributor.author","Wardelmann, Eva"],["dc.contributor.author","Buettner, Reinhard"],["dc.contributor.author","Hartmann, Wolfgang"],["dc.date.accessioned","2018-11-07T09:48:44Z"],["dc.date.available","2018-11-07T09:48:44Z"],["dc.date.issued","2015"],["dc.description.abstract","Liposarcomas (LS) are the most common malignant mesenchymal tumors, with an overall long-term mortality rate of 60%. LS comprise three major subtypes, i.e., well-differentiated/dedifferentiated liposarcoma (WDLS/DDLS), myxoid/round cell liposarcoma (MLS) and pleomorphic liposarcoma (PLS). Aiming at the preclinical identification of novel therapeutic options, we here investigate the functional significance of SRC in primary human LS and in LS-derived cell lines. Immunohistochemical and Western blot analyses reveal relevant levels of activated p-(Tyr416)-SRC in LS of the different subtypes with particular activation in MLS and PLS. Dysregulation of the SRC modifiers CSK and PTP1B was excluded as major reason for the activation of the kinase. Consistent siRNA-mediated knockdown of SRC or inhibition by the SRC inhibitor Dasatinib led to decreased proliferation of LS cell lines of the different subtypes, with MLS cells reacting particularly sensitive in MTT assays. Flow cytometric analyses revealed that this effect was due to a significant decrease in mitotic activity and an induction of apoptosis. SRC inhibition by Dasatinib resulted in dephosphorylation of SRC itself, its interacting partners FAK and IGF-IR as well as its downstream target AKT. Consistent with a particular role of SRC in cell motility, Dasatinib reduced the migratory and invasive potential of MLS cells in Boyden chamber and Matrigel chamber assays. In summary, we provide evidence that SRC activation plays an important role in LS biology and therefore represents a potential therapeutic target, particularly in MLS and PLS."],["dc.description.sponsorship","Deutsche Krebshilfe (KoSar-Sarcoma Net)"],["dc.identifier.doi","10.1002/ijc.29645"],["dc.identifier.isi","000362843000006"],["dc.identifier.pmid","26084847"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35366"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1097-0215"],["dc.relation.issn","0020-7136"],["dc.title","SRC inhibition represents a potential therapeutic strategy in liposarcoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]