Stockhammer, Florian

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Acta Neuropathologica Communications"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Christians, Arne"],["dc.contributor.author","Adel-Horowski, Antonia"],["dc.contributor.author","Banan, Rouzbeh"],["dc.contributor.author","Lehmann, Ulrich"],["dc.contributor.author","Bartels, Stephan"],["dc.contributor.author","Behling, Felix"],["dc.contributor.author","Barrantes-Freer, Alonso"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Rohde, Veit"],["dc.contributor.author","Stockhammer, Florian"],["dc.contributor.author","Hartmann, Christian"],["dc.date.accessioned","2020-12-10T18:41:23Z"],["dc.date.available","2020-12-10T18:41:23Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1186/s40478-019-0817-0"],["dc.identifier.eissn","2051-5960"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16626"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77568"],["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","The prognostic role of IDH mutations in homogeneously treated patients with anaplastic astrocytomas and glioblastomas"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","15"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neuro-Oncology"],["dc.bibliographiccitation.lastpage","22"],["dc.bibliographiccitation.volume","109"],["dc.contributor.author","Ahmadi, Rezvan"],["dc.contributor.author","Stockhammer, Florian"],["dc.contributor.author","Becker, Natalia"],["dc.contributor.author","Hohlen, Katarina"],["dc.contributor.author","Misch, Martin"],["dc.contributor.author","Christians, Arne"],["dc.contributor.author","Dictus, Christine"],["dc.contributor.author","Herold-Mende, Christel"],["dc.contributor.author","Capper, David"],["dc.contributor.author","Unterberg, Andreas"],["dc.contributor.author","von Deimling, Andreas"],["dc.contributor.author","Wick, Wolfgang"],["dc.contributor.author","Hartmann, Christian"],["dc.date.accessioned","2018-11-07T09:07:48Z"],["dc.date.available","2018-11-07T09:07:48Z"],["dc.date.issued","2012"],["dc.description.abstract","Mutations in the gene encoding isocitrate dehydrogenase 1 (IDH1) have been identified in approximately 70-80 % of astrocytomas and oligodendrogliomas of WHO grades II and III, and in secondary glioblastomas. In addition, a low incidence of IDH2 mutations has been detected in these tumors, and the occurence of IDH1 and IDH2 mutations is mutually exclusive. For patients with anaplastic gliomas and glioblastomas with IDH1 mutations, overall survival was significantly longer than for patients with wild-type tumours. However, the prognostic value of IDH1 in low-grade gliomas remains ambiguous. IDH1 codon 132 and IDH2 codon 172 mutation status were determined by direct sequencing for a retrospective series of 100 patients with histologically diagnosed Astrocytomas WHO Grad II (A II), and investigated for association with patient outcome. For the patient cohort analysed, median progression-free survival (PFS) was 44.6 months (95 %-CI 1.0-267.0), time to progression (median time to malignant progression (TtMP) was 74.9 months (95 %-CI 1.6-236.2), and median overall survival (OS) was 81.4 months (95 %-CI 5.5-274.8). IDH1 mutations were identified in 79 % of the patients. IDH2 mutations were not observed. Univariate and multivariate analysis revealed no association between IDH1 mutation status and PFS, TtMP, and OS. Furthermore, there were no significant differences regarding PFS, TtMP, and OS between patients with and without IDH1 mutations who did not receive adjuvant treatment. The prognostic value of IDH1 mutations in low-grade astrocytomas is rather low compared with that in high-grade gliomas."],["dc.identifier.doi","10.1007/s11060-012-0863-y"],["dc.identifier.isi","000306953100003"],["dc.identifier.pmid","22528790"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25885"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0167-594X"],["dc.title","No prognostic value of IDH1 mutations in a series of 100 WHO grade II astrocytomas"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","15"],["dc.bibliographiccitation.journal","Journal of Clinical Oncology"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Wick, Wolfgang"],["dc.contributor.author","Roth, Patrick"],["dc.contributor.author","Wiestler, Benedikt"],["dc.contributor.author","Hartmann, Christian"],["dc.contributor.author","Hau, Peter"],["dc.contributor.author","Nakamura, Makoto"],["dc.contributor.author","Stockhammer, Florian"],["dc.contributor.author","Sabel, Michael"],["dc.contributor.author","Koeppen, Susanne"],["dc.contributor.author","Ketter, Ralf"],["dc.contributor.author","Vajkoczy, Peter"],["dc.contributor.author","Eyupoglus, Ilker"],["dc.contributor.author","Kaendler, Stephen"],["dc.contributor.author","Kalff, Rolf"],["dc.contributor.author","Galldiks, Norbert"],["dc.contributor.author","Schmidt-Graf, Friederike"],["dc.contributor.author","von Deimling, Andreas"],["dc.contributor.author","Platten, Michael"],["dc.contributor.author","Reifenberger, Guido"],["dc.contributor.author","Weller, Michael"],["dc.date.accessioned","2018-11-07T09:57:08Z"],["dc.date.available","2018-11-07T09:57:08Z"],["dc.date.issued","2015"],["dc.identifier.isi","000358036900460"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37097"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Clinical Oncology"],["dc.publisher.place","Alexandria"],["dc.relation.conference","Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO)"],["dc.relation.eventlocation","Chicago, IL"],["dc.relation.issn","1527-7755"],["dc.relation.issn","0732-183X"],["dc.title","Long-term analysis of the NOA-04 randomized phase III trial of sequential radiochemotherapy of anaplastic glioma with PCV or temozolomide"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","55"],["dc.bibliographiccitation.journal","Diagnostic Pathology"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Behling, Felix"],["dc.contributor.author","Barrantes-Freer, Alonso"],["dc.contributor.author","Skardelly, Marco"],["dc.contributor.author","Nieser, Maike"],["dc.contributor.author","Christians, Arne"],["dc.contributor.author","Stockhammer, Florian"],["dc.contributor.author","Rohde, Veit"],["dc.contributor.author","Tatagiba, Marcos"],["dc.contributor.author","Hartmann, Christian"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Schittenhelm, Jens"],["dc.date.accessioned","2018-11-07T10:12:37Z"],["dc.date.available","2018-11-07T10:12:37Z"],["dc.date.issued","2016"],["dc.description.abstract","Background: Treatment options for oncological diseases have been enhanced by the advent of targeted therapies. The point mutation of the BRAF gene at codon 600 (BRAF V600E) is found in several tumor entities and can be approached with selective inhibitory antibodies. The BRAF inhibitor vemurafenib has demonstrated clinical efficacy in patients with BRAF V600E-mutant melanoma brain metastases and in other cancer diseases. Therefore the BRAF V600E mutation is a highly interesting oncological target in brain tumors. Methods: This study assesses the BRAF V600E mutation status in 969 intracranial neoplasms using a tissue microarray method and immunohistochemical staining with the mutation-specific VE-1 antibody, followed by sequencing of positively stained cases. Results: Out of 784 primary brain tumors seven cases with a BRAF V600E mutation were detected (7/784, 1 %). Six of these cases were neuroepithelial tumors (6/667, 1 %) encompassing 2 astrocytomas WHO grade II (2/42, 5 %), 1 gliosarcoma WHO grade IV (1/75, 1 %) and 3 glioblastomas WHO grade IV (3/312, 1 %). Interestingly, all three mutant glioblastomas showed epithelioid histopathological features. Patients with V600E mutated astrocytic tumors were significantly younger (mean age 15.3 years) than wildtype cases (58.2 years). Among three rhabdoid meningiomas, one case was mutated (1/3) while all other grade I-III meningiomas (1/116, 1 %) and all fifty vestibular schwannomas analyzed were of wildtype status. The vast majority of the BRAF V600E mutations were found in cerebral metastases of malignant melanomas and carcinomas (29/135, 22 %), with false-positive staining found in four breast cancer cases and two non-small-cell lung carcinoma (NSCLC) samples. Conclusions: Our data suggest routine screening for BRAF V600E mutations for glioblastomas WHO grade IV below the age of 30, especially in glioblastomas with epithelioid features and in all rhabdoid meningiomas WHO grade III. For colorectal carcinoma, thyroid cancer, malignant melanoma and gliomas BRAF V600E immunostaining is sufficient for screening purposes. We also recommend routine immunohistochemical staining followed by sequencing validation in rare CNS metastases or metastases of unknown primary. Immunohistochemical analysis using mutation-specific antibodies on tissue microarrays is a feasible, time-and cost-efficient approach to high-throughput screening for specific mutations in large tumor series but sequencing validation is necessary in unexpected cases."],["dc.identifier.doi","10.1186/s13000-016-0506-2"],["dc.identifier.isi","000379298900001"],["dc.identifier.pmid","27350555"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13365"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40275"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1746-1596"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Frequency of BRAF V600E mutations in 969 central nervous system neoplasms"],["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"]]

[["dc.bibliographiccitation.firstpage","e0229274"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","PLoS One"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Behling, Felix"],["dc.contributor.author","Barrantes-Freer, Alonso"],["dc.contributor.author","Behnes, Carl Ludwig"],["dc.contributor.author","Stockhammer, Florian"],["dc.contributor.author","Rohde, Veit"],["dc.contributor.author","Adel-Horowski, Antonia"],["dc.contributor.author","Rodríguez-Villagra, Odir Antonio"],["dc.contributor.author","Barboza, Miguel Angel"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Lehmann, Ulrich"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Hartmann, Christian"],["dc.contributor.editor","Hjelmeland, Anita B."],["dc.date.accessioned","2021-04-14T08:27:01Z"],["dc.date.available","2021-04-14T08:27:01Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1371/journal.pone.0229274"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82143"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1932-6203"],["dc.title","Expression of Olig2, Nestin, NogoA and AQP4 have no impact on overall survival in IDH-wildtype glioblastoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","194"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Seizure"],["dc.bibliographiccitation.lastpage","197"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Stockhammer, Florian"],["dc.contributor.author","Misch, Martin"],["dc.contributor.author","Helms, Hans-Joachim"],["dc.contributor.author","Lengler, Ulrike"],["dc.contributor.author","Prall, Friedrich"],["dc.contributor.author","von Deimling, Andreas"],["dc.contributor.author","Hartmann, Christian"],["dc.date.accessioned","2018-11-07T09:11:43Z"],["dc.date.available","2018-11-07T09:11:43Z"],["dc.date.issued","2012"],["dc.description.abstract","Introduction: Seizures are the most common initial symptom in patients with low-grade glioma and their occurrence strongly depends on the tumor location. The majority of low-grade gliomas reveal mutations in the genes encoding isocitrate-dehydrogenase 1 (IDH1) or 2 (IDH2). These mutations are associated with metabolic changes that are potentially epileptogenic. We investigated the correlation between IDH1/2 mutations and tumor localization and seizure as the initial symptom. Materials and methods: This retrospective study included patients with a diagnosis of WHO grade II astrocytoma and cortical infiltration and in whom initial symptoms were documented and biopsy tissue was available for 1DH1/2 analysis. IDH1/2 mutation analysis was performed by direct sequencing or by immunohistochemistry with an antibody which detects mutated protein IDH1 R132H. Sequencing was carried out if immunohistochemistry was negative. 1DH1/2 status was defined as mutated if either of these investigations were positive. Results: Seventy-nine patients were included. IDH1 or IDH2 mutation was present in 63 (80%) patients who on average were younger than patients without IDH1/2 mutation (40 vs. 47 years, p = 0.0331, t-test). IDH1/2 mutations were associated with frontal tumor location (p = 0.0202). All 12 tumors in the insula revealed IDH1/2 mutations. Seizure as the initial symptom was recorded in 57 (72%) patients and was associated with IDH1 or IDH2 mutation by multivariate analysis (OR 22.563, p = 0.0019). Conclusion: In WHO grade II astrocytomas, IDH1/2 mutations mostly occur in tumors infiltrating the frontal lobe. Seizure as the initial symptom is associated with IDH1 or IDH2 mutation. (C) 2011 British Epilepsy Association. Published by Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.seizure.2011.12.007"],["dc.identifier.isi","000302449700009"],["dc.identifier.pmid","22217666"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26783"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","W B Saunders Co Ltd"],["dc.relation.issn","1059-1311"],["dc.title","IDH1/2 mutations in WHO grade II astrocytomas associated with localization and seizure as the initial symptom"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1529"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Neuro-Oncology"],["dc.bibliographiccitation.lastpage","1537"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Wick, Wolfgang"],["dc.contributor.author","Roth, Patrick"],["dc.contributor.author","Hartmann, Christian"],["dc.contributor.author","Hau, Peter"],["dc.contributor.author","Nakamura, Makoto"],["dc.contributor.author","Stockhammer, Florian"],["dc.contributor.author","Sabel, Michael C."],["dc.contributor.author","Wick, Antje"],["dc.contributor.author","Koeppen, Susanne"],["dc.contributor.author","Ketter, Ralf"],["dc.contributor.author","Vajkoczy, Peter"],["dc.contributor.author","Eyupoglu, Ilker"],["dc.contributor.author","Kalff, Rolf"],["dc.contributor.author","Pietsch, Torsten"],["dc.contributor.author","Happold, Caroline"],["dc.contributor.author","Galldiks, Norbert"],["dc.contributor.author","Schmidt-Graf, Friederike"],["dc.contributor.author","Bamberg, Michael"],["dc.contributor.author","Reifenberger, Guido"],["dc.contributor.author","Platten, Michael"],["dc.contributor.author","von Deimling, Andreas"],["dc.contributor.author","Meisner, Christoph"],["dc.contributor.author","Wiestler, Benedikt"],["dc.contributor.author","Weller, Michael"],["dc.date.accessioned","2018-11-07T10:06:29Z"],["dc.date.available","2018-11-07T10:06:29Z"],["dc.date.issued","2016"],["dc.description.abstract","Background. Optimal treatment and precise classification for anaplastic glioma are needed. Methods. The objective for long-term follow-up of NOA-04 is to optimize the treatment sequence for patients with anaplastic gliomas. Patients were randomized 2: 1: 1 to receive the standard radiotherapy (RT) (arm A), procarbazine, lomustine and vincristine (PCV) (arm B1), or temozolomide (TMZ) (arm B2). Results. Primary endpoint was time-to-treatment-failure (TTF), defined as progression after 2 lines of therapy or any time before if no further therapy was administered. Exploratory analyses examined associations of molecular marker status with TTF, progression-free survival (PFS), and overall survival (OS). At 9.5 (95% CI: 8.6-10.2) years, no difference between arms (A vs B1/B2) was observed: median TTF (4.6 [3.4-5.1] y vs 4.4 [3.3-5.3) y), PFS (2.5 [1.3-3.5] y vs 2.7 [1.9-3.2] y), and OS (8 [5.5-10.3] y vs 6.5 [5.4-8.3] y). Oligodendroglial versus astrocytic histology-but more so the subgroups according to CpG island methylator phenotype (CIMP) and 1p/19q co-deletion status-revealed a strong prognostic value of CIMPpos with (CIMPcodel) versus without 1p/19 co-deletion (CIMPnon-codel) versus CIMPneg. but no differential efficacy of RT versus chemotherapy for any of the endpoints. PFS was better for PCV-than for TMZ-treated patients with CIMPcodel tumors (HR B1 vs B2 0.39 [0.17-0.92], P = .31). In CIMPneg. tumors, hypermethylation of the O6-methyl-guanyl-DNA methyltransferase promoter (MGMT) provided a risk reduction for PFS with chemotherapy. Conclusions. There is no differential activity of primary chemotherapy versus RT in any subgroup of anaplastic glioma. Molecular diagnosis is superior to histology. Trial Registration: clinicaltrials.gov Identifier: NCT00717210."],["dc.identifier.doi","10.1093/neuonc/now133"],["dc.identifier.isi","000387330300009"],["dc.identifier.pmid","27370396"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39103"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1523-5866"],["dc.relation.issn","1522-8517"],["dc.title","Long-term analysis of the NOA-04 randomized phase III trial of sequential radiochemotherapy of anaplastic glioma with PCV or temozolomide"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]