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.firstpage","449"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Histopathology"],["dc.bibliographiccitation.lastpage","459"],["dc.bibliographiccitation.volume","72"],["dc.contributor.author","Scheel, Andreas H"],["dc.contributor.author","Baenfer, Gudrun"],["dc.contributor.author","Baretton, Gustavo"],["dc.contributor.author","Dietel, Manfred"],["dc.contributor.author","Diezko, Rolf"],["dc.contributor.author","Henkel, Thomas"],["dc.contributor.author","Heukamp, Lukas C"],["dc.contributor.author","Jasani, Bharat"],["dc.contributor.author","Jöhrens, Korinna"],["dc.contributor.author","Kirchner, Thomas"],["dc.contributor.author","Lasitschka, Felix"],["dc.contributor.author","Petersen, Iver"],["dc.contributor.author","Reu, Simone"],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.contributor.author","Schirmacher, Peter"],["dc.contributor.author","Schwamborn, Kristina"],["dc.contributor.author","Sommer, Ulrich"],["dc.contributor.author","Stoss, Oliver"],["dc.contributor.author","Tiemann, Markus"],["dc.contributor.author","Warth, Arne"],["dc.contributor.author","Weichert, Wilko"],["dc.contributor.author","Wolf, Jürgen"],["dc.contributor.author","Büttner, Reinhard"],["dc.contributor.author","Rüschoff, Josef"],["dc.date.accessioned","2020-12-10T18:28:50Z"],["dc.date.available","2020-12-10T18:28:50Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1111/his.2018.72.issue-3"],["dc.identifier.issn","0309-0167"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/76422"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Interlaboratory concordance of PD-L1 immunohistochemistry for non-small-cell lung cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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","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"]]

[["dc.bibliographiccitation.firstpage","1266"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Journal of Thoracic Oncology"],["dc.bibliographiccitation.lastpage","1276"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Michels, Sebastian"],["dc.contributor.author","Massutí, Bartomeu"],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.contributor.author","Franklin, Jeremy"],["dc.contributor.author","Sebastian, Martin"],["dc.contributor.author","Felip, Enriqueta"],["dc.contributor.author","Grohé, Christian"],["dc.contributor.author","Rodriguez-Abreu, Delvys"],["dc.contributor.author","Abdulla, Diana S.Y."],["dc.contributor.author","Bischoff, Helge"],["dc.contributor.author","Brandts, Christian"],["dc.contributor.author","Carcereny, Enric"],["dc.contributor.author","Corral, Jesús"],["dc.contributor.author","Dingemans, Anne-Marie C."],["dc.contributor.author","Pereira, Eva"],["dc.contributor.author","Fassunke, Jana"],["dc.contributor.author","Fischer, Rieke N."],["dc.contributor.author","Gardizi, Masyar"],["dc.contributor.author","Heukamp, Lukas"],["dc.contributor.author","Insa, Amelia"],["dc.contributor.author","Kron, Anna"],["dc.contributor.author","Menon, Roopika"],["dc.contributor.author","Persigehl, Thorsten"],["dc.contributor.author","Reck, Martin"],["dc.contributor.author","Riedel, Richard"],["dc.contributor.author","Rothschild, Sacha I."],["dc.contributor.author","Scheel, Andreas H."],["dc.contributor.author","Scheffler, Matthias"],["dc.contributor.author","Schmalz, Petra"],["dc.contributor.author","Smit, Egbert F."],["dc.contributor.author","Limburg, Meike"],["dc.contributor.author","Provencio, Mariano"],["dc.contributor.author","Karachaliou, Niki"],["dc.contributor.author","Merkelbach-Bruse, Sabine"],["dc.contributor.author","Hellmich, Martin"],["dc.contributor.author","Nogova, Lucia"],["dc.contributor.author","Büttner, Reinhard"],["dc.contributor.author","Rosell, Rafael"],["dc.contributor.author","Wolf, Jürgen"],["dc.date.accessioned","2020-12-10T15:20:07Z"],["dc.date.available","2020-12-10T15:20:07Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1016/j.jtho.2019.03.020"],["dc.identifier.issn","1556-0864"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72563"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Safety and Efficacy of Crizotinib in Patients With Advanced or Metastatic ROS1-Rearranged Lung Cancer (EUCROSS): A European Phase II Clinical Trial"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","860532"],["dc.bibliographiccitation.journal","Case reports in oncological medicine"],["dc.bibliographiccitation.volume","2014"],["dc.contributor.author","Schultheis, Anne M."],["dc.contributor.author","Nguyen, Gia Phuong"],["dc.contributor.author","Ortmann, Monika"],["dc.contributor.author","Kruis, Wolfgang"],["dc.contributor.author","Büttner, Reinhard"],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.contributor.author","Markiefka, Birgid"],["dc.date.accessioned","2019-07-09T11:41:17Z"],["dc.date.available","2019-07-09T11:41:17Z"],["dc.date.issued","2014"],["dc.description.abstract","Primary squamous cell carcinoma of the pancreas is a rare malignant neoplasia, accounting for approximately 0.5-2% of all malignant pancreatic tumors. These lesions are characterized by poor prognosis. Here we report on a case of a 57-year-old female patient with known BRCA2 germline mutation presenting with primary squamous cell carcinoma of the pancreas as the only malignancy. The tumor was locally advanced at the first presentation but responded almost completely to neoadjuvant radio-chemotherapy. Our case highlights the facts (i) that pancreatic carcinomas belong to the tumor spectrum of patients with the BRCA2-associated hereditary breast and ovarian cancer syndrome (HBOC) and (ii) that tumors of the pancreas can represent the first or even the only manifestation of HBOC. Furthermore, this case of a nonkeratinizing squamous cell carcinoma indicates that HBOC-associated carcinomas of the pancreas might be characterized by a broader morphological spectrum than was previously thought. Since BRCA mutations cause deficiency of DNA double-strand breakage repair in tumors, neoadjuvant treatment regimens might become a reasonable option in HBOC-associated pancreatic carcinomas. To our knowledge, this is the first reported case of a primary pancreatic squamous cell carcinoma in a patient with this particular genetic background of BRCA2-associated HBOC."],["dc.identifier.doi","10.1155/2014/860532"],["dc.identifier.fs","611822"],["dc.identifier.pmid","24959366"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11917"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58395"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2090-6706"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","Squamous Cell Carcinoma of the Pancreas in a Patient with Germline BRCA2 Mutation-Response to Neoadjuvant Radiochemotherapy."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1530"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Pathology - Research and Practice"],["dc.bibliographiccitation.lastpage","1535"],["dc.bibliographiccitation.volume","213"],["dc.contributor.author","Petersen, Iver"],["dc.contributor.author","Dietel, Manfred"],["dc.contributor.author","Geilenkeuser, Wolf J."],["dc.contributor.author","Mireskandari, Masoud"],["dc.contributor.author","Weichert, Wilko"],["dc.contributor.author","Steiger, Katja"],["dc.contributor.author","Scheel, Andreas H."],["dc.contributor.author","Büttner, Reinhard"],["dc.contributor.author","Schirmacher, Peter"],["dc.contributor.author","Warth, Arne"],["dc.contributor.author","Lasitschka, Felix"],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.contributor.author","Kirchner, Thomas"],["dc.contributor.author","Reu, Simone"],["dc.contributor.author","Kreipe, Hans"],["dc.contributor.author","Länger, Florian"],["dc.contributor.author","Tiemann, Markus"],["dc.contributor.author","Schulte, Christoph"],["dc.contributor.author","Jöhrens, Korinna"],["dc.date.accessioned","2020-12-10T15:20:56Z"],["dc.date.available","2020-12-10T15:20:56Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1016/j.prp.2017.09.021"],["dc.identifier.issn","0344-0338"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72862"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","EGFR immunohistochemistry as biomarker for antibody-based therapy of squamous NSCLC – Experience from the first ring trial of the German Quality Assurance Initiative for Pathology (QuIP ® )"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]