Barrantes-Freer, Alonso

[["dc.bibliographiccitation.firstpage","181"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","The Journal of Physiology"],["dc.bibliographiccitation.lastpage","196"],["dc.bibliographiccitation.volume","593"],["dc.contributor.author","Mortensen, Lena Sünke"],["dc.contributor.author","Schmidt, Hartmut"],["dc.contributor.author","Farsi, Zohreh"],["dc.contributor.author","Barrantes-Freer, Alonso"],["dc.contributor.author","Rubio, María E."],["dc.contributor.author","Ufartes, Roser"],["dc.contributor.author","Eilers, Jens"],["dc.contributor.author","Sakaba, Takeshi"],["dc.contributor.author","Stühmer, Walter"],["dc.contributor.author","Pardo, Luis A."],["dc.date.accessioned","2019-07-09T11:42:47Z"],["dc.date.available","2019-07-09T11:42:47Z"],["dc.date.issued","2014"],["dc.description.abstract","The voltage-gated potassium channel KV10.1 (Eag1) is widely expressed in the mammalian brain, but its physiological function is not yet understood. Previous studies revealed highest expression levels in hippocampus and cerebellumand suggested a synaptic localization of the channel. The distinct activation kinetics of KV10.1 indicate a role during repetitive activity of the cell.Here, we confirmthe synaptic localization of KV10.1 both biochemically and functionally and that the channel is sufficiently fast at physiological temperature to take part in repolarization of the action potential (AP).We studied the role of the channel in cerebellar physiology using patch clamp and two-photon Ca2+ imaging in KV10.1-deficient and wild-type mice. The excitability and action potential waveformrecorded at granule cell somata was unchanged, while Ca2+ influx into axonal boutons was enhanced in mutants in response to stimulation with three APs, but not after a single AP. Furthermore, mutants exhibited a frequency-dependent increase in facilitation at the parallel fibre–Purkinje cell synapse at high firing rates. We propose that KV10.1 acts as a modulator of local AP shape specifically during high-frequency burst firing when other potassium channels suffer cumulative inactivation."],["dc.identifier.doi","10.1113/jphysiol.2014.281600"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13714"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58742"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","0022-3751"],["dc.rights","CC BY-NC-ND 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/3.0"],["dc.title","KV 10.1 opposes activity-dependent increase in Ca2+ influx into the presynaptic terminal of the parallel fibre-Purkinje cell synapse"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1381"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Physiological Reviews"],["dc.bibliographiccitation.lastpage","1431"],["dc.bibliographiccitation.volume","99"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Timmler, Sebastian"],["dc.contributor.author","Barrantes-Freer, Alonso"],["dc.contributor.author","Simons, Mikael"],["dc.date.accessioned","2020-12-10T18:37:40Z"],["dc.date.available","2020-12-10T18:37:40Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1152/physrev.00031.2018"],["dc.identifier.eissn","1522-1210"],["dc.identifier.issn","0031-9333"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16423"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77059"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Myelin in the Central Nervous System: Structure, Function, and Pathology"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["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.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.artnumber","e0130519"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Barrantes-Freer, Alonso"],["dc.contributor.author","Renovanz, Mirjam"],["dc.contributor.author","Eich, Marcus"],["dc.contributor.author","Braukmann, Alina"],["dc.contributor.author","Sprang, Bettina"],["dc.contributor.author","Spirin, Pavel"],["dc.contributor.author","Pardo, Luis A."],["dc.contributor.author","Giese, Alf"],["dc.contributor.author","Kim, Ella L."],["dc.date.accessioned","2018-11-07T09:55:48Z"],["dc.date.available","2018-11-07T09:55:48Z"],["dc.date.issued","2015"],["dc.description.abstract","A transmembrane protein CD133 has been implicated as a marker of stem-like glioma cells and predictor for therapeutic response in malignant brain tumours. CD133 expression is commonly evaluated by using antibodies specific for the AC133 epitope located in one of the extracellular domains of membrane-bound CD133. There is conflicting evidence regarding the significance of the AC133 epitope as a marker for identifying stem-like glioma cells and predicting the degree of malignancy in glioma cells. The reasons for discrepant results between different studies addressing the role of CD133/AC133 in gliomas are unclear. A possible source for controversies about CD133/AC133 is the widespread assumption that expression patterns of the AC133 epitope reflect linearly those of the CD133 protein. Consequently, the readouts from AC133 assessments are often interpreted in terms of the CD133 protein. The purpose of this study is to determine whether and to what extent do the readouts obtained with anti-AC133 antibody correspond to the level of CD133 protein expressed in stem-like glioma cells. Our study reveals for the first time that CD133 expressed on the surface of glioma cells is poorly immunoreactive for AC133. Furthermore, we provide evidence that the level of CD133 occupancy on the surface of glioma cells fluctuates during the cell cycle. Our results offer a new explanation for numerous inconsistencies regarding the biological and clinical significance of CD133/AC133 in human gliomas and call for caution in interpreting the lack or presence of AC133 epitope in glioma cells."],["dc.identifier.doi","10.1371/journal.pone.0130519"],["dc.identifier.isi","000356567500111"],["dc.identifier.pmid","26086074"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11954"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36830"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","CD133 Expression Is Not Synonymous to Immunoreactivity for AC133 and Fluctuates throughout the Cell Cycle in Glioma Stem-Like Cells"],["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","15"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","34"],["dc.bibliographiccitation.volume","134"],["dc.contributor.author","Lagumersindez-Denis, Nielsen"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Mack, Matthias"],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","van der Meer, Franziska"],["dc.contributor.author","Reinert, Marie-Christine"],["dc.contributor.author","Hollasch, Heiko"],["dc.contributor.author","Flach, Anne"],["dc.contributor.author","Bruehl, Hilke"],["dc.contributor.author","Cullen, Eilish"],["dc.contributor.author","Schlumbohm, Christina"],["dc.contributor.author","Fuchs, Eberhard"],["dc.contributor.author","Linington, Christopher"],["dc.contributor.author","Barrantes-Freer, Alonso"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Wegner, Christiane"],["dc.contributor.author","Liebetanz, David"],["dc.contributor.author","Prinz, Marco R."],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Nessler, Stefan"],["dc.date.accessioned","2018-11-07T10:22:07Z"],["dc.date.available","2018-11-07T10:22:07Z"],["dc.date.issued","2017"],["dc.description.abstract","Cortical demyelination is a widely recognized hallmark of multiple sclerosis (MS) and correlate of disease progression and cognitive decline. The pathomechanisms initiating and driving gray matter damage are only incompletely understood. Here, we determined the infiltrating leukocyte subpopulations in 26 cortical demyelinated lesions of biopsied MS patients and assessed their contribution to cortical lesion formation in a newly developed mouse model. We find that conformation-specific anti-myelin antibodies contribute to cortical demyelination even in the absence of the classical complement pathway. T cells and natural killer cells are relevant for intracortical type 2 but dispensable for subpial type 3 lesions, whereas CCR2(+) monocytes are required for both. Depleting CCR2(+) monocytes in marmoset monkeys with experimental autoimmune encephalomyelitis using a novel humanized CCR2 targeting antibody translates into significantly less cortical demyelination and disease severity. We conclude that biologics depleting CCR2(+) monocytes might be attractive candidates for preventing cortical lesion formation and ameliorating disease progression in MS."],["dc.identifier.doi","10.1007/s00401-017-1706-x"],["dc.identifier.isi","000403235900002"],["dc.identifier.pmid","28386765"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14713"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42218"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Springer"],["dc.relation.issn","1432-0533"],["dc.relation.issn","0001-6322"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Differential contribution of immune effector mechanisms to cortical demyelination in multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3170"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","International Journal of Cancer"],["dc.bibliographiccitation.lastpage","3183"],["dc.bibliographiccitation.volume","146"],["dc.contributor.author","Blazquez, Raquel"],["dc.contributor.author","Rietkötter, Eva"],["dc.contributor.author","Wenske, Britta"],["dc.contributor.author","Wlochowitz, Darius"],["dc.contributor.author","Sparrer, Daniela"],["dc.contributor.author","Vollmer, Elena"],["dc.contributor.author","Müller, Gunnar"],["dc.contributor.author","Seegerer, Julia"],["dc.contributor.author","Sun, Xueni"],["dc.contributor.author","Dettmer, Katja"],["dc.contributor.author","Barrantes‐Freer, Alonso"],["dc.contributor.author","Stange, Lena"],["dc.contributor.author","Utpatel, Kirsten"],["dc.contributor.author","Bleckmann, Annalen"],["dc.contributor.author","Treiber, Hannes"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Schulz, Matthias"],["dc.contributor.author","Reimelt, Christian"],["dc.contributor.author","Hackl, Christina"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Büyüktas, Deram"],["dc.contributor.author","Siam, Laila"],["dc.contributor.author","Balkenhol, Marko"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Kube, Dieter"],["dc.contributor.author","Krahn, Michael P."],["dc.contributor.author","Proescholdt, Martin A."],["dc.contributor.author","Riemenschneider, Markus J."],["dc.contributor.author","Evert, Matthias"],["dc.contributor.author","Oefner, Peter J."],["dc.contributor.author","Klein, Chistoph A."],["dc.contributor.author","Hanisch, Uwe K."],["dc.contributor.author","Binder, Claudia"],["dc.contributor.author","Pukrop, Tobias"],["dc.date.accessioned","2019-12-09T11:26:05Z"],["dc.date.accessioned","2021-10-27T13:21:49Z"],["dc.date.available","2019-12-09T11:26:05Z"],["dc.date.available","2021-10-27T13:21:49Z"],["dc.date.issued","2020"],["dc.description.abstract","More than half of all brain metastases show infiltrating rather than displacing growth at the macro-metastasis/organ parenchyma interface (MMPI), a finding associated with shorter survival. The lymphoid enhancer-binding factor-1 (LEF1) is an epithelial-mesenchymal transition (EMT) transcription factor that is commonly overexpressed in brain-colonizing cancer cells. Here, we overexpressed LEF1 in an in vivo breast cancer brain colonization model. It shortened survival, albeit without engaging EMT at the MMPI. By differential proteome analysis, we identified a novel function of LEF1 as a regulator of the glutathione (GSH) system, the principal cellular redox buffer. LEF1 overexpression also conferred resistance against therapeutic GSH depletion during brain colonization and improved management of intracellular ROS. We conclude that besides EMT, LEF1 facilitates metastasis by improving the antioxidative capacity of epithelial breast cancer cells, in particular during colonization of the brain parenchyma."],["dc.identifier.doi","10.1002/ijc.32742"],["dc.identifier.eissn","1097-0215"],["dc.identifier.issn","0020-7136"],["dc.identifier.pmid","31626715"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16874"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92047"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.eissn","1097-0215"],["dc.relation.issn","1097-0215"],["dc.relation.issn","0020-7136"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","LEF1 supports metastatic brain colonization by regulating glutathione metabolism and increasing ROS resistance in breast cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","105012"],["dc.bibliographiccitation.journal","Neurobiology of Disease"],["dc.bibliographiccitation.volume","143"],["dc.contributor.author","Lazarov, Elinor"],["dc.contributor.author","Hillebrand, Merle"],["dc.contributor.author","Schröder, Simone"],["dc.contributor.author","Ternka, Katharina"],["dc.contributor.author","Hofhuis, Julia"],["dc.contributor.author","Ohlenbusch, Andreas"],["dc.contributor.author","Barrantes-Freer, Alonso"],["dc.contributor.author","Pardo, Luis A."],["dc.contributor.author","Fruergaard, Marlene U."],["dc.contributor.author","Nissen, Poul"],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Gärtner, Jutta"],["dc.contributor.author","Rosewich, Hendrik"],["dc.date.accessioned","2021-04-14T08:23:22Z"],["dc.date.available","2021-04-14T08:23:22Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1016/j.nbd.2020.105012"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17488"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/80889"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","0969-9961"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Comparative analysis of alternating hemiplegia of childhood and rapid-onset dystonia-parkinsonism ATP1A3 mutations reveals functional deficits, which do not correlate with disease severity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","213"],["dc.bibliographiccitation.journal","BMC Cancer"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Martinez, Ramon"],["dc.contributor.author","Carmona, F. Javier"],["dc.contributor.author","Vizoso, Miguel"],["dc.contributor.author","Rohde, Veit"],["dc.contributor.author","Kirsch, Matthias"],["dc.contributor.author","Schackert, Gabriele"],["dc.contributor.author","Ropero, Santiago"],["dc.contributor.author","Paulus, Werner"],["dc.contributor.author","Barrantes, Alonso"],["dc.contributor.author","Gomez, Antonio"],["dc.contributor.author","Esteller, Manel"],["dc.date.accessioned","2018-11-07T09:42:29Z"],["dc.date.available","2018-11-07T09:42:29Z"],["dc.date.issued","2014"],["dc.description.abstract","Background: Pleomorphic xanthoastrocytoma (PXA) is a rare WHO grade II tumor accounting for less than 1% of all astrocytomas. Malignant transformation into PXA with anaplastic features, is unusual and correlates with poorer outcome of the patients. Methods: Using a DNA methylation custom array, we have quantified the DNA methylation level on the promoter sequence of 807 cancer-related genes of WHO grade II (n = 11) and III PXA (n = 2) and compared to normal brain tissue (n = 10) and glioblastoma (n = 87) samples. DNA methylation levels were further confirmed on independent samples by pyrosequencing of the promoter sequences. Results: Increasing DNA promoter hypermethylation events were observed in anaplastic PXA as compared with grade II samples. We further validated differential hypermethylation of CD81, HCK, HOXA5, ASCL2 and TES on anaplastic PXA and grade II tumors. Moreover, these epigenetic alterations overlap those described in glioblastoma patients, suggesting common mechanisms of tumorigenesis. Conclusions: Even taking into consideration the small size of our patient populations, our data strongly suggest that epigenome wide profiling of PXA is a valuable tool to identify methylated genes, which may play a role in the malignant progression of PXA. These methylation alterations may provide useful biomarkers for decision-making in those patients with low-grade PXA displaying a high risk of malignant transformation."],["dc.description.sponsorship","Cellex Foundation (Spain); ICREA"],["dc.identifier.doi","10.1186/1471-2407-14-213"],["dc.identifier.isi","000334533400001"],["dc.identifier.pmid","24650279"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10070"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33963"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1471-2407"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","DNA methylation alterations in grade II- and anaplastic pleomorphic xanthoastrocytoma"],["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","29254"],["dc.bibliographiccitation.issue","30"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","29267"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Siam, Laila"],["dc.contributor.author","Bleckmann, Annalen"],["dc.contributor.author","Chaung, Han-Ning"],["dc.contributor.author","Mohr, Alexander"],["dc.contributor.author","Klemm, Florian"],["dc.contributor.author","Barrantes-Freer, Alonso"],["dc.contributor.author","Blazquez, Raquel"],["dc.contributor.author","Wolff, Hendrik Andreas"],["dc.contributor.author","Lueke, Florian"],["dc.contributor.author","Rohde, Veit"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Pukrop, Tobias"],["dc.date.accessioned","2018-11-07T09:50:20Z"],["dc.date.available","2018-11-07T09:50:20Z"],["dc.date.issued","2015"],["dc.description.abstract","The current approach to brain metastases resection is macroscopic removal of metastasis until reaching the glial pseudo-capsule (gross total resection (GTR)). However, autopsy studies demonstrated infiltrating metastatic cells into the parenchyma at the metastasis/brain parenchyma (M/BP)-interface. Aims/Methods: To analyze the astrocyte reaction and metastatic infiltration pattern at the M/BP-interface with an organotypic brain slice coculture system. Secondly, to evaluate the significance of infiltrating metastatic tumor cells in a prospective biopsy study. Therefore, after GTR, biopsies were obtained from the brain parenchyma beyond the glial pseudo-capsule and analyzed histomorphologically. Results: The coculture revealed three types of cancer cell infiltration. Interestingly, the astrocyte reaction was significantly different in the coculture with a benign, neuroectodermal-derived cell line. In the prospective biopsy study 58/167 (34.7%) samples revealed infiltrating metastatic cells. Altogether, 25/39 patients (64.1%) had proven to exhibit infiltration in at least one biopsy specimen with significant impact on survival (OS) (3.4 HR; p = 0.009; 2-year OS was 6.6% versus 43.5%). Exceptionally, in the non-infiltrating cohort three patients were long-term survivors. Conclusions: Metastatic infiltration has a significant impact on prognosis. Secondly, the astrocyte reaction at the M/BP-interface is heterogeneous and supports our previous concept of the organ-specific defense against metastatic (organ-foreign) cells."],["dc.identifier.doi","10.18632/oncotarget.4201"],["dc.identifier.isi","000363183200062"],["dc.identifier.pmid","26299612"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13618"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35687"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Impact Journals Llc"],["dc.relation.issn","1949-2553"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","The metastatic infiltration at the metastasis/brain parenchyma-interface is very heterogeneous and has a significant impact on survival in a prospective study"],["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"]]