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","825"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","835"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Kübler, Kirsten"],["dc.contributor.author","Heinenberg, Sally"],["dc.contributor.author","Rudlowski, Christian"],["dc.contributor.author","Keyver-Paik, Mignon-Denise"],["dc.contributor.author","Abramian, Alina"],["dc.contributor.author","Merkelbach-Bruse, Sabine"],["dc.contributor.author","Büttner, Reinhard"],["dc.contributor.author","Kuhn, Walther"],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.date.accessioned","2019-07-09T11:42:38Z"],["dc.date.available","2019-07-09T11:42:38Z"],["dc.date.issued","2015-01-20"],["dc.description.abstract","Cervical carcinoma develops from preneoplasia by a multistep process. Although most low-grade dysplastic lesions will regress without intervention and even high-grade changes exhibit a substantial rate of regression, a small percentage of dysplasia will progress over time. Thus, indicators are needed to estimate the biological risk and to help avoid overtreatment in women who desire to preserve fertility. In addition to the classical biomarkers, PCR-ELISA-determined HPV genotype and immunohistochemically assessed p16INK4a and Ki-67 expression, cells with integrated HPV and copy number gain of TERC and c-myc were quantified in a panel of 104 benign, intraepithelial neoplastic (CIN I, II, III) and cancerous lesions using fluorescence in situ hybridization. Optimal cut-off values were calculated; Kaplan-Meier curves and a Cox proportional hazard regression model were used to evaluate prognostic signatures. The assay reliably identified HPV integration, TERC and c-myc copy number gain as determined by comparisons with established biomarkers. All biomarker levels increased with the progression of the disease. However, only c-myc copy number gain independently prognosticated a low probability of dysplastic regression. Our results suggest that c-myc plays a key role in the process of dysplastic transformation and might thus be exploited for treatment and follow-up decision-making of cervical dysplasia."],["dc.identifier.doi","10.18632/oncotarget.2706"],["dc.identifier.fs","611817"],["dc.identifier.pmid","25596731"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13610"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58711"],["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","Carcinoma, Squamous Cell"],["dc.subject.mesh","Cervical Intraepithelial Neoplasia"],["dc.subject.mesh","Disease Progression"],["dc.subject.mesh","Female"],["dc.subject.mesh","Gene Dosage"],["dc.subject.mesh","Genes, myc"],["dc.subject.mesh","Genotype"],["dc.subject.mesh","Humans"],["dc.subject.mesh","Prognosis"],["dc.subject.mesh","Treatment Outcome"],["dc.subject.mesh","Uterine Cervical Neoplasms"],["dc.title","c-myc copy number gain is a powerful prognosticator of disease outcome in cervical dysplasia."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]