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Schildhaus, Hans-Ulrich
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Schildhaus, Hans-Ulrich
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Schildhaus, Hans-Ulrich
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Schildhaus, H.-U.
Schildhaus, Hans Ulrich
Schildhaus, H. U.
Schildhaus, Hans U.
Schildhaus, Hans
Schildhaus, H.
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2016Journal Article [["dc.bibliographiccitation.firstpage","3028"],["dc.bibliographiccitation.issue","15_suppl"],["dc.bibliographiccitation.journal","Journal of Clinical Oncology"],["dc.bibliographiccitation.lastpage","3028"],["dc.bibliographiccitation.volume","34"],["dc.contributor.author","Scheel, Andreas H."],["dc.contributor.author","Dietel, Manfred"],["dc.contributor.author","Heukamp, Lukas C."],["dc.contributor.author","Jöhrens, Korinna"],["dc.contributor.author","Kirchner, Thomas"],["dc.contributor.author","Reu, Simone"],["dc.contributor.author","Ruschoff, Josef"],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.contributor.author","Schirmacher, Peter"],["dc.contributor.author","Tiemann, Markus"],["dc.contributor.author","Warth, Arne"],["dc.contributor.author","Weichert, Wilko"],["dc.contributor.author","Fischer, Rieke Nila"],["dc.contributor.author","Wolf, Juergen"],["dc.contributor.author","Buettner, Reinhard"],["dc.date.accessioned","2020-12-10T18:41:30Z"],["dc.date.available","2020-12-10T18:41:30Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.1200/JCO.2016.34.15_suppl.3028"],["dc.identifier.eissn","1527-7755"],["dc.identifier.issn","0732-183X"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77597"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Diagnostic PD-L1 immunohistochemistry in NSCLC: Results of the first German harmonization study."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2017Review [["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"]]Details DOI PMID PMC WOS2013Journal Article [["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"]]Details DOI PMID PMC WOS2015Conference Abstract [["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"]]Details WOS2016Journal Article [["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"]]Details DOI2016Journal Article [["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"]]Details DOI PMID PMC WOS2014Journal Article [["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"]]Details DOI PMID PMC WOS2015Journal Article [["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"]]Details DOI PMID PMC WOS2017Journal Article [["dc.bibliographiccitation.firstpage","e20508"],["dc.bibliographiccitation.issue","15_suppl"],["dc.bibliographiccitation.journal","Journal of Clinical Oncology"],["dc.bibliographiccitation.lastpage","e20508"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Scheel, Andreas H."],["dc.contributor.author","Bänfer, Gudrun"],["dc.contributor.author","Baretton, Gustavo Bruno"],["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","Petersen, Iver"],["dc.contributor.author","Reu, Simone"],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.contributor.author","Schirmacher, Peter"],["dc.contributor.author","Tiemann, Markus"],["dc.contributor.author","Warth, Arne"],["dc.contributor.author","Weichert, Wilko"],["dc.contributor.author","Wolf, Juergen"],["dc.contributor.author","Rüschoff, Josef"],["dc.contributor.author","Buettner, Reinhard"],["dc.date.accessioned","2020-12-10T18:41:34Z"],["dc.date.available","2020-12-10T18:41:34Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1200/JCO.2017.35.15_suppl.e20508"],["dc.identifier.eissn","1527-7755"],["dc.identifier.issn","0732-183X"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77614"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Interlaboratory-concordance of PD-L1 IHC for NSCLC."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2016Journal Article [["dc.bibliographiccitation.firstpage","1165"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Modern Pathology"],["dc.bibliographiccitation.lastpage","1172"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Scheel, Andreas Hans"],["dc.contributor.author","Dietel, Manfred"],["dc.contributor.author","Heukamp, Lukas Carl"],["dc.contributor.author","Joehrens, Korinna"],["dc.contributor.author","Kirchner, Thomas"],["dc.contributor.author","Reu, Simone"],["dc.contributor.author","Rueschoff, Josef"],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.contributor.author","Schirmacher, Peter"],["dc.contributor.author","Tiemann, Markus"],["dc.contributor.author","Warth, Arne"],["dc.contributor.author","Weichert, Wilko"],["dc.contributor.author","Fischer, Rieke N."],["dc.contributor.author","Wolf, Juergen"],["dc.contributor.author","Buettner, Reinhard"],["dc.date.accessioned","2018-11-07T10:08:00Z"],["dc.date.available","2018-11-07T10:08:00Z"],["dc.date.issued","2016"],["dc.description.abstract","Immunohistochemistry of the PD-L1 protein may be predictive for anti-PD-1 and anti-PD-L1 immunotherapy in pulmonary adenocarcinoma and in clinically unselected cohorts of so-called non-small-cell lung cancer. Several PD-L1 immunohistochemistry assays with custom reagents and scoring-criteria are developed in parallel. Biomarker testing and clinical decision making would profit from harmonized PD-L1 diagnostics. To assess interobserver concordance and PD-L1 immunohistochemistry staining patterns, 15 pulmonary carcinoma resection specimens (adenocarcinoma: n = 11, squamous-cell carcinoma: n = 4) were centrally stained with the assays 28-8, 22C3, SP142, and SP263 according to clinical trial protocols. The slides were evaluated independently by nine pathologists. Proportions of PD-L1-positive carcinoma cells and immune cells were scored according to a 6-step system that integrates the criteria employed by the four PD-L1 immunohistochemistry assays. Proportion scoring of PD-L1-positive carcinoma cells showed moderate interobserver concordance coefficients for the 6-step Kscoring system (Light's kappa = 0.47-0.50). The integrated dichotomous proportion cut-offs (>= 1, >= 5, >= 10, >= 50%) showed good concordance coefficients (kappa = 0.6-0.8). Proportion scoring of PD-L1-positive immune cells yielded low interobserver concordance coefficients both for the 6-step-score (kappa<0.2) and the dichotomous cut-offs (kappa = 0.12-0.25). The assays 28-8 and 22C3 stained similar proportions of carcinoma cells in 12 of 15 cases. SP142 stained fewer carcinoma cells compared to 28-8, 22C3, and SP263 in four cases, whereas SP263 stained more carcinoma cells in nine cases. SP142 and SP263 stained immune cells more intensely. The data indicate that carcinoma cells can be reproducibly scored in PD-L1 immunohistochemistry for pulmonary adenocarcinoma and squamous-cell carcinoma. No differences in interobserver concordance were noticed among the tested assays. The scoring of immune cells yielded low concordance rates and might require specific standardization. The four tested PD-L1 assays did not show comparable staining patterns in all cases. Thus, studies that correlate staining patterns and response to immunotherapy are required to test the significance of the observed differences."],["dc.description.sponsorship","Bristol-Myers Squibb; MSD; Roche; AstraZeneca"],["dc.identifier.doi","10.1038/modpathol.2016.117"],["dc.identifier.isi","000384548100004"],["dc.identifier.pmid","27389313"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39393"],["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","Harmonized PD-L1 immunohistochemistry for pulmonary squamous-cell and adenocarcinomas"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS