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.journal","Modern Pathology"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Schildhaus, H-U"],["dc.contributor.author","Binot, Elke"],["dc.contributor.author","Buttner, R."],["dc.contributor.author","Tancheva-Poor, I."],["dc.contributor.author","Wardelmann, Eva"],["dc.date.accessioned","2018-11-07T09:44:20Z"],["dc.date.available","2018-11-07T09:44:20Z"],["dc.date.issued","2014"],["dc.format.extent","28A"],["dc.identifier.isi","000331502200099"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34370"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.publisher.place","New york"],["dc.relation.conference","103rd Annual Meeting of the United-States-and-Canadian-Academy-of-Pathology (USCAP)"],["dc.relation.eventlocation","San Diego, CA"],["dc.relation.issn","1530-0285"],["dc.relation.issn","0893-3952"],["dc.title","Validation of Break Apart FISH Probes for the Detection of COL1A1-PDGFB Rearrangements in Dermatofibrosarcoma Protuberans"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Laboratory Investigation"],["dc.bibliographiccitation.volume","94"],["dc.contributor.author","Schildhaus, H-U"],["dc.contributor.author","Binot, Elke"],["dc.contributor.author","Buttner, R."],["dc.contributor.author","Tancheva-Poor, I."],["dc.contributor.author","Wardelmann, Eva"],["dc.date.accessioned","2018-11-07T09:44:19Z"],["dc.date.available","2018-11-07T09:44:19Z"],["dc.date.issued","2014"],["dc.format.extent","28A"],["dc.identifier.isi","000331155800099"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34365"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.publisher.place","New york"],["dc.relation.conference","103rd Annual Meeting of the United-States-and-Canadian-Academy-of-Pathology (USCAP)"],["dc.relation.eventlocation","San Diego, CA"],["dc.relation.issn","1530-0307"],["dc.relation.issn","0023-6837"],["dc.title","Validation of Break Apart FISH Probes for the Detection of COL1A1-PDGFB Rearrangements in Dermatofibrosarcoma Protuberans"],["dc.type","conference_abstract"],["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","214"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Modern Pathology"],["dc.bibliographiccitation.lastpage","221"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Schultheis, Anne Maria"],["dc.contributor.author","Bos, Marc"],["dc.contributor.author","Schmitz, Katja"],["dc.contributor.author","Wilsberg, Lea"],["dc.contributor.author","Binot, Elke"],["dc.contributor.author","Wolf, Juergen"],["dc.contributor.author","Buettner, Reinhard"],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.date.accessioned","2018-11-07T09:44:29Z"],["dc.date.available","2018-11-07T09:44:29Z"],["dc.date.issued","2014"],["dc.description.abstract","Small-cell lung cancer (SCLC) comprises about 13-15% of all lung cancers, and more than 29400 new cases have been diagnosed in the United States in the year 2012. SCLC is a biologically complex tumor typically occurring in heavy smokers. Its medical treatment has almost remained unchanged over the last decades and selected treatment options have not been established so far, mainly due to the lack of targetable genetic alterations. In this study we analyzed a cohort of 307 SCLC samples for fibroblast growth factor receptor 1 (FGFR1) amplification using a dual color FISH probe. FGFR1 status was correlated with clinical data. FGFR1 amplifications were observed in 5.6% of evaluable pulmonary SCLCs. Most of them (93%) fulfilled the criteria for high-level amplification and only one case showed low-level amplification. Amplification patterns were homogenous in the entire tumor area without occurrence of any 'hot spot' areas. FGFR1 amplification status was not associated with age, sex, stage, smoking status or overall survival. FGFR1 amplification analysis by FISH analysis in SCLC is, under respect of certain technical issues, applicable in the routine clinical setting. However, the FGFR1 amplification patterns in SCLC differs strongly from the previously described FGFR1 amplification pattern in squamous cell carcinoma of the lung, as positive SCLC harbor mostly homogeneous high-level amplifications. We provide evidence that an estimated number of 1640 newly diagnosed FGFR1-positive SCLC cases in the United States annually could benefit from targeted therapy. Therefore, we recommend including SCLC in the screening for ongoing clinical trials with FGFR1 inhibitors."],["dc.identifier.doi","10.1038/modpathol.2013.141"],["dc.identifier.isi","000330910100006"],["dc.identifier.pmid","23887299"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34408"],["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","Fibroblast growth factor receptor 1 (FGFR1) amplification is a potential therapeutic target in small-cell lung cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","907"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Clinical Cancer Research"],["dc.bibliographiccitation.lastpage","915"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.contributor.author","Schultheis, Anne Maria"],["dc.contributor.author","Rüschoff, Josef R."],["dc.contributor.author","Binot, Elke"],["dc.contributor.author","Merkelbach-Bruse, Sabine"],["dc.contributor.author","Fassunke, Jana"],["dc.contributor.author","Schulte, Wolfgang"],["dc.contributor.author","Ko, Yon-Dschun"],["dc.contributor.author","Schlesinger, Andreas"],["dc.contributor.author","Bos, Marc"],["dc.contributor.author","Gardizi, Masyar"],["dc.contributor.author","Engel-Riedel, Walburga"],["dc.contributor.author","Brockmann, Michael"],["dc.contributor.author","Serke, Monika Heidi"],["dc.contributor.author","Gerigk, Ulrich"],["dc.contributor.author","Hekmat, Khosro"],["dc.contributor.author","Frank, Konrad F."],["dc.contributor.author","Reiser, Marcel"],["dc.contributor.author","Schulz, Holger"],["dc.contributor.author","Krüger, Stefan"],["dc.contributor.author","Stoelben, Erich"],["dc.contributor.author","Zander, Thomas"],["dc.contributor.author","Wolf, Jürgen"],["dc.contributor.author","Buettner, Reinhard"],["dc.date.accessioned","2018-11-07T10:00:53Z"],["dc.date.available","2018-11-07T10:00:53Z"],["dc.date.issued","2015"],["dc.description.abstract","Purpose: MET is a potential therapeutic target in lung cancer and both MET tyrosine kinase inhibitors and monoclonal antibodies have entered clinical trials. MET signaling can be activated by various mechanisms, including gene amplification. In this study, we aimed to investigate MET amplification status in adeno- and squamous cell carcinomas of the lung. We propose clearly defined amplification scores and provide epidemiologic data on MET amplification in lung cancer. Experimental Design: We evaluated the prevalence of increased MET gene copy numbers in 693 treatment-naive cancers by FISH, defined clear cutoff criteria, and correlated FISH results to MET IHC. Results: Two thirds (67%) of lung cancers do not have gains in MET gene copy numbers, whereas 3% show a clear-cut high-level amplification (MET/centromer7 ratio =2.0 or average gene copy number per nucleus =6.0 or =10% of tumor cells containing =15 MET copies). The remaining cases can be subdivided into intermediate- (6%) and low-level gains (24%). Importantly, MET amplifications occur at equal frequencies in squamous and adenocarcinomas without or with EGFR or KRAS mutations. Conclusion: MET amplification is not a mutually exclusive genetic event in therapy-naive non-small cell lung cancer. Our data suggest that it might be useful to determine MET amplification (i) before EGFR inhibitor treatment to identify possible primary resistance to anti-EGFR treatment, and (ii) to select cases that harbor KRAS mutations additionally to MET amplification and, thus, may not benefit from MET inhibition. Furthermore, our study provides comprehensive epidemiologic data for upcoming trials with various MET inhibitors. (C) 2014 AACR."],["dc.identifier.doi","10.1158/1078-0432.CCR-14-0450"],["dc.identifier.isi","000349851200029"],["dc.identifier.pmid","25492085"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37902"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Cancer Research"],["dc.relation.issn","1557-3265"],["dc.relation.issn","1078-0432"],["dc.title","MET Amplification Status in Therapy-Naive Adeno- and Squamous Cell Carcinomas 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.journal","Modern Pathology"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.contributor.author","Binot, Elke"],["dc.contributor.author","Wolf, Juergen"],["dc.contributor.author","Buettner, Reinhard"],["dc.contributor.author","Schmitz, Katja"],["dc.date.accessioned","2018-11-07T10:18:50Z"],["dc.date.available","2018-11-07T10:18:50Z"],["dc.date.issued","2016"],["dc.format.extent","482A"],["dc.identifier.isi","000369270703070"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41531"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.publisher.place","New york"],["dc.relation.conference","105th Annual Meeting of the United-States-and-Canadian-Academy-of-Pathology"],["dc.relation.eventlocation","Seattle, WA"],["dc.relation.issn","1530-0307"],["dc.relation.issn","0023-6837"],["dc.title","Validation of a Simplified Approach to Detect ALK Translocations in Lung Cancer Samples by FISH"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","573"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Human Pathology"],["dc.bibliographiccitation.lastpage","582"],["dc.bibliographiccitation.volume","45"],["dc.contributor.author","Kuenstlinger, Helen"],["dc.contributor.author","Binot, Elke"],["dc.contributor.author","Merkelbach-Bruse, Sabine"],["dc.contributor.author","Huss, Sebastian"],["dc.contributor.author","Wardelmann, Eva"],["dc.contributor.author","Buettner, Reinhard"],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.date.accessioned","2018-11-07T09:43:24Z"],["dc.date.available","2018-11-07T09:43:24Z"],["dc.date.issued","2014"],["dc.description.abstract","The mutational status of KIT and PDGFRA is highly relevant for prognosis and therapy prediction in gastrointestinal stromal tumors (GIST). PDGFRA exon 18 mutations have direct therapeutic implications since it is crucial to distinguish mutations associated with sensitivity to tyrosine kinase inhibitors from those causing primary resistance, eg, the most common exon 18 mutation p.D842V. In response to a growing demand for reliable, faster and more sensitive methods we established and validated a high-resolution melting (BRM) assay for PDGFRA exon 18. A total of 159 GIST samples were comparatively analyzed by FIRM and direct Sanger sequencing. We demonstrate that BRM provides highly reliable mutational results with higher sensitivity and shorter time to diagnosis compared to Sanger sequencing. We determined the sensitivity threshold of FIRM at 6% of mutated alleles. PDGFRA exon 18 wild-type status and the most common p.D842V resistance mutation (together representing >90% of the cases) can be detected specifically by FIRM. Other rare mutations can be pre-screened by FIRM and afterwards determined precisely by DNA sequencing. In this way we detected four novel mutations in PDGFRA exon 18, two of which were associated with an aggressive clinical course. Including these new mutations, we provide a comprehensive overview of all 60 currently known subtypes of PDGFRA exon 18 mutations in GIST. Seven of them (accounting for about 75% of all exon 18-mutated GISTs) are reported to be resistant to imatinib. However, there are at least 10 other mutations which are regarded as sensitive to tyrosine kinase inhibitors. (C) 2014 Elsevier Inc. All rights reserved."],["dc.description.sponsorship","Novartis Oncology"],["dc.identifier.doi","10.1016/j.humpath.2013.10.025"],["dc.identifier.isi","000331854400017"],["dc.identifier.pmid","24444465"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34178"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","W B Saunders Co-elsevier Inc"],["dc.relation.issn","1532-8392"],["dc.relation.issn","0046-8177"],["dc.title","High-resolution melting analysis is a sensitive diagnostic tool to detect imatinib-resistant and imatinib-sensitive PDGFRA exon 18 mutations in gastrointestinal stromal tumors"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]