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.artnumber","13"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","BMC Cancer"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Ihle, Michaela A."],["dc.contributor.author","Fassunke, Jana"],["dc.contributor.author","König, Katharina"],["dc.contributor.author","Grünewald, Inga"],["dc.contributor.author","Schlaak, Max"],["dc.contributor.author","Kreuzberg, Nicole"],["dc.contributor.author","Tietze, Lothar"],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.contributor.author","Büttner, Reinhard"],["dc.contributor.author","Merkelbach-Bruse, Sabine"],["dc.date.accessioned","2019-07-09T11:39:42Z"],["dc.date.available","2019-07-09T11:39:42Z"],["dc.date.issued","2014"],["dc.description.abstract","Background The approval of vemurafenib in the US 2011 and in Europe 2012 improved the therapy of not resectable or metastatic melanoma. Patients carrying a substitution of valine to glutamic acid at codon 600 (p.V600E) or a substitution of valine to leucine (p.V600K) in BRAF show complete or partial response. Therefore, the precise identification of the underlying somatic mutations is essential. Herein, we evaluate the sensitivity, specificity and feasibility of six different methods for the detection of BRAF mutations. Methods Samples harboring p.V600E mutations as well as rare mutations in BRAF exon 15 were compared to wildtype samples. DNA was extracted from formalin-fixed paraffin-embedded tissues by manual micro-dissection and automated extraction. BRAF mutational analysis was carried out by high resolution melting (HRM) analysis, pyrosequencing, allele specific PCR, next generation sequencing (NGS) and immunohistochemistry (IHC). All mutations were independently reassessed by Sanger sequencing. Due to the limited tumor tissue available different numbers of samples were analyzed with each method (82, 72, 60, 72, 49 and 82 respectively). Results There was no difference in sensitivity between the HRM analysis and Sanger sequencing (98%). All mutations down to 6.6% allele frequency could be detected with 100% specificity. In contrast, pyrosequencing detected 100% of the mutations down to 5% allele frequency but exhibited only 90% specificity. The allele specific PCR failed to detect 16.3% of the mutations eligible for therapy with vemurafenib. NGS could analyze 100% of the cases with 100% specificity but exhibited 97.5% sensitivity. IHC showed once cross-reactivity with p.V600R but was a good amendment to HRM. Conclusion Therefore, at present, a combination of HRM and IHC is recommended to increase sensitivity and specificity for routine diagnostic to fulfill the European requirements concerning vemurafenib therapy of melanoma patients."],["dc.identifier.doi","10.1186/1471-2407-14-13"],["dc.identifier.fs","603375"],["dc.identifier.pmid","24410877"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10053"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58025"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Comparison of high resolution melting analysis, pyrosequencing, next generation sequencing and immunohistochemistry to conventional Sanger sequencing for the detection of p.V600E and non-p.V600E BRAF mutations"],["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"]]

[["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","1468"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Modern Pathology"],["dc.bibliographiccitation.lastpage","1477"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.contributor.author","Deml, Karl-Friedrich"],["dc.contributor.author","Schmitz, Katja"],["dc.contributor.author","Meiboom, Maren"],["dc.contributor.author","Binot, Elke"],["dc.contributor.author","Hauke, Sven"],["dc.contributor.author","Merkelbach-Bruse, Sabine"],["dc.contributor.author","Buettner, Reinhard"],["dc.date.accessioned","2018-11-07T09:18:10Z"],["dc.date.available","2018-11-07T09:18:10Z"],["dc.date.issued","2013"],["dc.description.abstract","Reliable detection of anaplastic lymphoma kinase (ALK) rearrangements is a prerequisite for personalized treatment of lung cancer patients, as ALK rearrangements represent a predictive biomarker for the therapy with specific tyrosine kinase inhibitors. Currently, fluorescent in situ hybridization (FISH) is considered to be the standard method for assessing formalin-fixed and paraffin-embedded tissue for ALK inversions and translocations. However, FISH requires a specialized equipment, the signals fade rapidly and it is difficult to detect overall morphology and tumor heterogeneity. Chromogenic in situ hybridization (CISH) has been successfully introduced as an alternative test for the detection of several genetic aberrations. This study validates a newly developed ALK CISH assay by comparing FISH and CISH signal patterns in lung cancer samples with and without ALK rearrangements. One hundred adenocarcinomas of the lung were included in this study, among them 17 with known ALK rearrangement. FISH and CISH were carried out and evaluated according to the manufacturers' recommendations. For both assays, tumors were considered positive if >= 15% of tumor cells showed either isolated 3' signals or break-apart patterns or a combination of both. A subset of tumors was exemplarily examined by using a novel EML4 (echinoderm microtubule-associated protein-like 4) CISH probe. Red, green and fusion CISH signals were clearcut and different signal patterns were easily recognized. The percentage of aberrant tumor cells was statistically highly correlated (P<0.001) between FISH and CISH. On the basis of 86 samples that were evaluable by ALK CISH, we found a 100% sensitivity and 100% specificity of this assay. Furthermore, EML4 rearrangements could be recognized by CISH. CISH is a highly reliable, sensitive and specific method for the detection of ALK gene rearrangements in pulmonary adenocarcinomas. Our results suggest that CISH might serve as a suitable alternative to FISH, which is the current gold standard."],["dc.description.sponsorship","Lung Cancer Group Cologne (LCGC)"],["dc.identifier.doi","10.1038/modpathol.2013.95"],["dc.identifier.isi","000326686700007"],["dc.identifier.pmid","23743932"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28344"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1530-0285"],["dc.relation.issn","0893-3952"],["dc.title","Chromogenic in situ hybridization is a reliable assay for detection of ALK rearrangements in adenocarcinomas of the lung"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Journal of Thoracic Oncology"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Scheel, Andreas Hans"],["dc.contributor.author","Schmitz, Katja"],["dc.contributor.author","Wilsberg, Lea"],["dc.contributor.author","Fischer, Rieke N."],["dc.contributor.author","Merkelbach-Bruse, Sabine"],["dc.contributor.author","Binot, Elke"],["dc.contributor.author","Plenker, Dennis"],["dc.contributor.author","Wolf, Juergen"],["dc.contributor.author","Tsuta, Koji"],["dc.contributor.author","Kohno, Takashi"],["dc.contributor.author","Thomas, Roman K."],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.contributor.author","Buettner, Reinhard"],["dc.date.accessioned","2018-11-07T09:51:52Z"],["dc.date.available","2018-11-07T09:51:52Z"],["dc.date.issued","2015"],["dc.format.extent","S702"],["dc.identifier.isi","000370365103353"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35997"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.publisher.place","New york"],["dc.relation.issn","1556-1380"],["dc.relation.issn","1556-0864"],["dc.title","Prevalence of NRG1 fusions in Caucasian NSCLC patients determined by fluorescence in situ hybridisation"],["dc.type","conference_abstract"],["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","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.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"]]