Grabe, Niels

[["dc.bibliographiccitation.firstpage","1489"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Anticancer Research"],["dc.bibliographiccitation.lastpage","1496"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Schmoch, Thomas"],["dc.contributor.author","Gal, Zoltan"],["dc.contributor.author","Mock, Andreas"],["dc.contributor.author","Mossemann, Jan"],["dc.contributor.author","Lahrmann, Bernd"],["dc.contributor.author","Grabe, Niels"],["dc.contributor.author","Schmezer, Peter"],["dc.contributor.author","Lasitschka, Felix"],["dc.contributor.author","Beckhove, Philipp"],["dc.contributor.author","Unterberg, Andreas"],["dc.contributor.author","Herold-Mende, Christel"],["dc.date.accessioned","2022-05-02T09:02:43Z"],["dc.date.available","2022-05-02T09:02:43Z"],["dc.date.issued","2016-04"],["dc.description.abstract","Recently, anti-tumourigenic effects of all-trans-retinoic-acid (ATRA) on glioblastoma stem cells were demonstrated. Therefore we investigated if these beneficial effects could be enhanced by co-medication with epigenetic drugs such as the histone deacetylase (HDAC) inhibitor suberoylanilide hydroxamic acid (SAHA) or the DNA-methyltransferase inhibitor 5-aza-2'deoxycytidine (5-AZA)."],["dc.identifier.pmid","27069124"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/107543"],["dc.language.iso","en"],["dc.relation.eissn","1791-7530"],["dc.title","Combined Treatment of ATRA with Epigenetic Drugs Increases Aggressiveness of Glioma Xenografts"],["dc.type","journal_article"],["dc.type.internalPublication","no"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","170"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","BMC Medicine"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Jungk, Christine"],["dc.contributor.author","Mock, Andreas"],["dc.contributor.author","Exner, Janina"],["dc.contributor.author","Geisenberger, Christoph"],["dc.contributor.author","Warta, Rolf"],["dc.contributor.author","Capper, David"],["dc.contributor.author","Abdollahi, Amir"],["dc.contributor.author","Friauf, Sara"],["dc.contributor.author","Lahrmann, Bernd"],["dc.contributor.author","Grabe, Niels"],["dc.contributor.author","Beckhove, Philipp"],["dc.contributor.author","von Deimling, Andreas"],["dc.contributor.author","Unterberg, Andreas"],["dc.contributor.author","Herold-Mende, Christel"],["dc.date.accessioned","2022-04-29T14:54:16Z"],["dc.date.available","2022-04-29T14:54:16Z"],["dc.date.issued","2016"],["dc.description.abstract","The spatial relationship of glioblastoma (GBM) to the subventricular zone (SVZ) is associated with inferior patient survival. However, the underlying molecular phenotype is largely unknown. We interrogated an SVZ-dependent transcriptome and potential location-specific prognostic markers."],["dc.identifier.doi","10.1186/s12916-016-0710-7"],["dc.identifier.pmid","27782828"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/107126"],["dc.language.iso","en"],["dc.relation.issn","1741-7015"],["dc.title","Spatial transcriptome analysis reveals Notch pathway-associated prognostic markers in IDH1 wild-type glioblastoma involving the subventricular zone"],["dc.type","journal_article"],["dc.type.internalPublication","no"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","419"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","434"],["dc.bibliographiccitation.volume","130"],["dc.contributor.author","Geisenberger, Christoph"],["dc.contributor.author","Mock, Andreas"],["dc.contributor.author","Warta, Rolf"],["dc.contributor.author","Rapp, Carmen"],["dc.contributor.author","Schwager, Christian"],["dc.contributor.author","Korshunov, Andrey"],["dc.contributor.author","Nied, Ann-Katrin"],["dc.contributor.author","Capper, David"],["dc.contributor.author","Brors, Benedikt"],["dc.contributor.author","Jungk, Christine"],["dc.contributor.author","Jones, David"],["dc.contributor.author","Collins, V. Peter"],["dc.contributor.author","Ichimura, Koichi"],["dc.contributor.author","Bäcklund, L. Magnus"],["dc.contributor.author","Schnabel, Elena"],["dc.contributor.author","Mittelbron, Michel"],["dc.contributor.author","Lahrmann, Bernd"],["dc.contributor.author","Zheng, Siyuan"],["dc.contributor.author","Verhaak, Roel G. W."],["dc.contributor.author","Grabe, Niels"],["dc.contributor.author","Pfister, Stefan M."],["dc.contributor.author","Hartmann, Christian"],["dc.contributor.author","von Deimling, Andreas"],["dc.contributor.author","Debus, Jürgen"],["dc.contributor.author","Unterberg, Andreas"],["dc.contributor.author","Abdollahi, Amir"],["dc.contributor.author","Herold-Mende, Christel"],["dc.date.accessioned","2022-05-02T08:58:48Z"],["dc.date.available","2022-05-02T08:58:48Z"],["dc.date.issued","2015-09"],["dc.description.abstract","Glioblastoma (GBM) is a devastating tumor and few patients survive beyond 3 years. Defining the molecular determinants underlying long-term survival is essential for insights into tumor biology and biomarker identification. We therefore investigated homogeneously treated, IDH (wt) long-term (LTS, n = 10) and short-term survivors (STS, n = 6) by microarray transcription profiling. While there was no association of clinical parameters and molecular subtypes with long-term survival, STS tumors were characterized by differential polarization of infiltrating microglia with predominance of the M2 phenotype detectable both on the mRNA and protein level. Furthermore, transcriptional signatures of LTS and STS predicted patient outcome in a large, IDH (wt) cohort (n = 468). Interrogation of overlapping genomic alterations identified concurrent gain of chromosomes 19 and 20 as a favorable prognostic marker. The strong association of this co-gain with survival was validated by aCGH in a second, independent cohort (n = 124). Finally, FISH and gene expression data revealed gains to constitute low-amplitude, clonal events with a strong impact on transcription. In conclusion, these findings provide important insights into the manipulation of the innate immune system by particularly aggressive GBM tumors. Furthermore, we genomically characterize a previously unknown, clinically relevant subgroup of glioblastoma, which can easily be identified through modern neuropathological workup."],["dc.identifier.doi","10.1007/s00401-015-1427-y"],["dc.identifier.pmid","25931051"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/107529"],["dc.language.iso","en"],["dc.relation.eissn","1432-0533"],["dc.relation.issn","0001-6322"],["dc.title","Molecular profiling of long-term survivors identifies a subgroup of glioblastoma characterized by chromosome 19/20 co-gain"],["dc.type","journal_article"],["dc.type.internalPublication","no"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","23"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","The Journal of Pathology"],["dc.bibliographiccitation.lastpage","33"],["dc.bibliographiccitation.volume","234"],["dc.contributor.author","Campos, Benito"],["dc.contributor.author","Gal, Zoltan"],["dc.contributor.author","Baader, Aline"],["dc.contributor.author","Schneider, Tilman"],["dc.contributor.author","Sliwinski, Christopher"],["dc.contributor.author","Gassel, Kristina"],["dc.contributor.author","Bageritz, Josephine"],["dc.contributor.author","Grabe, Niels"],["dc.contributor.author","von Deimling, Andreas"],["dc.contributor.author","Beckhove, Philipp"],["dc.contributor.author","Mogler, Carolin"],["dc.contributor.author","Goidts, Violaine"],["dc.contributor.author","Unterberg, Andreas"],["dc.contributor.author","Eckstein, Volker"],["dc.contributor.author","Herold-Mende, Christel"],["dc.date.accessioned","2022-05-02T08:59:04Z"],["dc.date.available","2022-05-02T08:59:04Z"],["dc.date.issued","2014-09"],["dc.description.abstract","Cancer cells with enhanced self-renewal capacity influence tumour growth in glioblastoma. So far, a variety of surrogate markers have been proposed to enrich these cells, emphasizing the need to devise new characterization methods. Here, we screen a large panel of glioblastoma cultures (n = 21) cultivated under stem cell-permissive conditions and identify several cell lines with enhanced self-renewal capacity. These cell lines are capable of matrix-independent growth and form fast-growing, orthotopic tumours in mice. Employing isolation, re-plating, and label-retention techniques, we show that self-renewal potential of individual cells is partitioned asymmetrically between daughter cells in a robust and cell line-specific fashion. This yields populations of fast- and slow-cycling cells, which differ in the expression of cell cycle-associated transcripts. Intriguingly, fast-growing cells keep their slow-cycling counterparts in a reversible state of quiescence associated with high chemoresistance. Our results suggest that two different subpopulations of tumour cells contribute to aberrant growth and tumour recurrence after therapy in glioblastoma."],["dc.identifier.doi","10.1002/path.4366"],["dc.identifier.pmid","24756862"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/107533"],["dc.language.iso","en"],["dc.relation.eissn","1096-9896"],["dc.relation.issn","0022-3417"],["dc.title","Aberrant self-renewal and quiescence contribute to the aggressiveness of glioblastoma"],["dc.type","journal_article"],["dc.type.internalPublication","no"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","697313"],["dc.bibliographiccitation.journal","The Scientific World Journal"],["dc.bibliographiccitation.volume","2012"],["dc.contributor.author","Schüle, Rebecca"],["dc.contributor.author","Dictus, Christine"],["dc.contributor.author","Campos, Benito"],["dc.contributor.author","Wan, Feng"],["dc.contributor.author","Felsberg, Jörg"],["dc.contributor.author","Ahmadi, Rezvan"],["dc.contributor.author","Centner, Franz-Simon"],["dc.contributor.author","Grabe, Niels"],["dc.contributor.author","Reifenberger, Guido"],["dc.contributor.author","Bermejo, Justo L."],["dc.contributor.author","Unterberg, Andreas"],["dc.contributor.author","Herold-Mende, Christel"],["dc.date.accessioned","2022-04-29T14:55:53Z"],["dc.date.available","2022-04-29T14:55:53Z"],["dc.date.issued","2012"],["dc.description.abstract","Aberrant wnt pathway activation through cytoplasmic stabilization of β-catenin is crucial for the development of various human malignancies. In gliomagenesis, the role of canonical (i.e., β-catenin-dependent) signalling is largely unknown. Here, we studied canonical wnt pathway activation in 15 short-term cultures from high-grade gliomas and potential pathomechanisms leading to cytoplasmic β-catenin accumulation. Furthermore, we assessed the prognostic relevance of β-catenin expression in a tissue microarray comprising 283 astrocytomas. Expression of β-catenin, its transcriptional cofactors TCF-1 and TCF-4 as well as GSK-3β and APC, constituents of the β-catenin degradation complex was confirmed by RT-PCR in all cultures. A cytoplasmic β-catenin pool was detectable in 13/15 cultures leading to some transcriptional activity assessed by luciferase reporter gene assay in 8/13. Unlike other malignancies, characteristic mutations of β-catenin and APC leading to cytoplasmic stabilization of β-catenin were excluded by direct sequencing or protein truncation test. In patient tissues, β-catenin expression was directly and its degradation product's (β-catenin-P654) expression was inversely correlated with WHO grade. Increased β-catenin expression and low β-catenin-P654 expression were associated with shorter survival. Altogether, we report on potential canonical wnt pathway activation in high-grade gliomas and demonstrate that β-catenin expression in astrocytomas is associated with increased malignancy and adverse outcome."],["dc.identifier.doi","10.1100/2012/697313"],["dc.identifier.pmid","22919349"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/107150"],["dc.language.iso","en"],["dc.relation.issn","1537-744X"],["dc.title","Potential canonical wnt pathway activation in high-grade astrocytomas"],["dc.type","journal_article"],["dc.type.internalPublication","no"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","297"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","316"],["dc.bibliographiccitation.volume","134"],["dc.contributor.author","Rapp, Carmen"],["dc.contributor.author","Warta, Rolf"],["dc.contributor.author","Stamova, Slava"],["dc.contributor.author","Nowrouzi, Ali"],["dc.contributor.author","Geisenberger, Christoph"],["dc.contributor.author","Gal, Zoltan"],["dc.contributor.author","Roesch, Saskia"],["dc.contributor.author","Dettling, Steffen"],["dc.contributor.author","Juenger, Simone"],["dc.contributor.author","Bucur, Mariana"],["dc.contributor.author","Jungk, Christine"],["dc.contributor.author","DaoTrong, Philip"],["dc.contributor.author","Ahmadi, Rezvan"],["dc.contributor.author","Sahm, Felix"],["dc.contributor.author","Reuss, David"],["dc.contributor.author","Fermi, Valentina"],["dc.contributor.author","Herpel, Esther"],["dc.contributor.author","Eckstein, Volker"],["dc.contributor.author","Grabe, Niels"],["dc.contributor.author","Schramm, Christoph"],["dc.contributor.author","Weigand, Markus A."],["dc.contributor.author","Debus, Juergen"],["dc.contributor.author","von Deimling, Andreas"],["dc.contributor.author","Unterberg, Andreas"],["dc.contributor.author","Abdollahi, Amir"],["dc.contributor.author","Beckhove, Philipp"],["dc.contributor.author","Herold-Mende, Christel"],["dc.date.accessioned","2022-05-02T08:58:39Z"],["dc.date.available","2022-05-02T08:58:39Z"],["dc.date.issued","2017"],["dc.description.abstract","Glioblastoma (GBM) is a highly aggressive brain tumor and still remains incurable. Among others, an immature subpopulation of self-renewing and therapy-resistant tumor cells-often referred to as glioblastoma stem-like cells (GSCs)-has been shown to contribute to disease recurrence. To target these cells personalized immunotherapy has gained a lot of interest, e.g. by reactivating pre-existing anti-tumor immune responses against GSC antigens. To identify T cell targets commonly presented by GSCs and their differentiated counterpart, we used a proteomics-based separation of GSC proteins in combination with a T cell activation assay. Altogether, 713 proteins were identified by LC-ESI-MS/MS mass spectrometry. After a thorough filtering process, 32 proteins were chosen for further analyses. Immunogenicity of corresponding peptides was tested ex vivo. A considerable number of these antigens induced T cell responses in GBM patients but not in healthy donors. Moreover, most of them were overexpressed in primary GBM and also highly expressed in recurrent GBM tissues. Interestingly, expression of the most frequent T cell target antigens could also be confirmed in quiescent, slow-cycling GSCs isolated in high purity by the DEPArray technology. Finally, for a subset of these T cell target antigens, an association between expression levels and higher T cell infiltration as well as an increased expression of positive immune modulators was observed. In summary, we identified novel immunogenic proteins, which frequently induce tumor-specific T cell responses in GBM patients and were also detected in vitro in therapy-resistant quiescent, slow-cycling GSCs. Stable expression of these T cell targets in primary and recurrent GBM support their suitability for future clinical use."],["dc.identifier.doi","10.1007/s00401-017-1702-1"],["dc.identifier.pmid","28332095"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/107527"],["dc.language.iso","en"],["dc.relation.eissn","1432-0533"],["dc.relation.issn","0001-6322"],["dc.title","Identification of T cell target antigens in glioblastoma stem-like cells using an integrated proteomics-based approach in patient specimens"],["dc.type","journal_article"],["dc.type.internalPublication","no"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1953"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","The American Journal of Pathology"],["dc.bibliographiccitation.lastpage","1964"],["dc.bibliographiccitation.volume","178"],["dc.contributor.author","Campos, Benito"],["dc.contributor.author","Centner, Franz-Simon"],["dc.contributor.author","Bermejo, Justo Lorenzo"],["dc.contributor.author","Ali, Ramadan"],["dc.contributor.author","Dorsch, Katharina"],["dc.contributor.author","Wan, Feng"],["dc.contributor.author","Felsberg, Jörg"],["dc.contributor.author","Ahmadi, Rezvan"],["dc.contributor.author","Grabe, Niels"],["dc.contributor.author","Reifenberger, Guido"],["dc.contributor.author","Unterberg, Andreas"],["dc.contributor.author","Burhenne, Jürgen"],["dc.contributor.author","Herold-Mende, Christel"],["dc.date.accessioned","2022-05-02T08:58:27Z"],["dc.date.available","2022-05-02T08:58:27Z"],["dc.date.issued","2011-05"],["dc.description.abstract","Undifferentiated cell populations may influence tumor growth in malignant glioma. We investigated potential disruptions in the retinoic acid (RA) differentiation pathway that could lead to a loss of differentiation capacity, influencing patient prognosis. Expression of key molecules belonging to the RA differentiation pathway was analyzed in 283 astrocytic gliomas and was correlated with tumor proliferation, tumor differentiation, and patient survival. In addition, in situ concentrations of retinoids were measured in tumors, and RA signaling events were studied in vitro. Unlike other tumors, in gliomas expression of most RA signaling molecules increased with malignancy and was associated with augmented intratumoral retinoid levels in high-grade gliomas. Aberrantly expressed RA signaling molecules included i) the retinol-binding protein CRBP1, which facilitates cellular retinoid uptake; ii) ALDH1A1, capable of activating RA precursors; iii) the RA-degrading enzyme CYP26B1; and iv) the RA-binding protein FABP5, which can inhibit RA-induced differentiation. In contrast, expression of the RA-binding protein CRABP2, which fosters differentiation, was decreased in high-grade tumors. Moreover, expression of CRBP1 correlated with tumor proliferation, and FABP5 expression correlated with an undifferentiated tumor phenotype. CRBP1 and ALDH1A1 were independent prognostic markers for adverse patient survival. Our data indicate a complex and clinically relevant deregulation of RA signaling, which seems to be a central event in glioma pathogenesis."],["dc.identifier.doi","10.1016/j.ajpath.2011.01.051"],["dc.identifier.pmid","21514413"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/107524"],["dc.language.iso","en"],["dc.relation.eissn","1525-2191"],["dc.relation.issn","0002-9440"],["dc.title","Aberrant expression of retinoic acid signaling molecules influences patient survival in astrocytic gliomas"],["dc.type","journal_article"],["dc.type.internalPublication","no"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","14551"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","14568"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Schmidt, Melissa"],["dc.contributor.author","Mock, Andreas"],["dc.contributor.author","Jungk, Christine"],["dc.contributor.author","Sahm, Felix"],["dc.contributor.author","Ull, Anna Theresa"],["dc.contributor.author","Warta, Rolf"],["dc.contributor.author","Lamszus, Katrin"],["dc.contributor.author","Gousias, Konstantinos"],["dc.contributor.author","Ketter, Ralf"],["dc.contributor.author","Roesch, Saskia"],["dc.contributor.author","Rapp, Carmen"],["dc.contributor.author","Schefzyk, Sebastian"],["dc.contributor.author","Urbschat, Steffi"],["dc.contributor.author","Lahrmann, Bernd"],["dc.contributor.author","Kessler, Almuth F"],["dc.contributor.author","Löhr, Mario"],["dc.contributor.author","Senft, Christian"],["dc.contributor.author","Grabe, Niels"],["dc.contributor.author","Reuss, David"],["dc.contributor.author","Beckhove, Philipp"],["dc.contributor.author","Westphal, Manfred"],["dc.contributor.author","von Deimling, Andreas"],["dc.contributor.author","Unterberg, Andreas"],["dc.contributor.author","Simon, Matthias"],["dc.contributor.author","Herold-Mende, Christel"],["dc.date.accessioned","2022-04-29T14:53:23Z"],["dc.date.available","2022-04-29T14:53:23Z"],["dc.date.issued","2016-03-22"],["dc.description.abstract","Meningiomas are frequent central nervous system tumors. Although most meningiomas are benign (WHO grade I) and curable by surgery, WHO grade II and III tumors remain therapeutically challenging due to frequent recurrence. Interestingly, relapse also occurs in some WHO grade I meningiomas. Hence, we investigated the transcriptional features defining aggressive (recurrent, malignantly progressing or WHO grade III) meningiomas in 144 cases. Meningiomas were categorized into non-recurrent (NR), recurrent (R), and tumors undergoing malignant progression (M) in addition to their WHO grade. Unsupervised transcriptomic analysis in 62 meningiomas revealed transcriptional profiles lining up according to WHO grade and clinical subgroup. Notably aggressive subgroups (R+M tumors and WHO grade III) shared a large set of differentially expressed genes (n=332; p<0.01, FC>1.25). In an independent multicenter validation set (n=82), differential expression of 10 genes between WHO grades was confirmed. Additionally, among WHO grade I tumors differential expression between NR and aggressive R+M tumors was affirmed for PTTG1, AURKB, ECT2, UBE2C and PRC1, while MN1 and LEPR discriminated between NR and R+M WHO grade II tumors. Univariate survival analysis revealed a significant association with progression-free survival for PTTG1, LEPR, MN1, ECT2, PRC1, COX10, UBE2C expression, while multivariate analysis identified a prediction for PTTG1 and LEPR mRNA expression independent of gender, WHO grade and extent of resection. Finally, stainings of PTTG1 and LEPR confirmed malignancy-associated protein expression changes. In conclusion, based on the so far largest study sample of WHO grade III and recurrent meningiomas we report a comprehensive transcriptional landscape and two prognostic markers."],["dc.identifier.doi","10.18632/oncotarget.7396"],["dc.identifier.pmid","26894859"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/107113"],["dc.language.iso","en"],["dc.relation.issn","1949-2553"],["dc.title","Transcriptomic analysis of aggressive meningiomas identifies PTTG1 and LEPR as prognostic biomarkers independent of WHO grade"],["dc.type","journal_article"],["dc.type.internalPublication","no"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","136"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Biomarkers"],["dc.bibliographiccitation.lastpage","143"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Wan, Feng"],["dc.contributor.author","Herold-Mende, Christel"],["dc.contributor.author","Campos, Benito"],["dc.contributor.author","Centner, Franz-Simon"],["dc.contributor.author","Dictus, Christine"],["dc.contributor.author","Becker, Natalia"],["dc.contributor.author","Devens, Frauke"],["dc.contributor.author","Mogler, Carolin"],["dc.contributor.author","Felsberg, Jörg"],["dc.contributor.author","Grabe, Niels"],["dc.contributor.author","Reifenberger, Guido"],["dc.contributor.author","Lichter, Peter"],["dc.contributor.author","Unterberg, Andreas"],["dc.contributor.author","Bermejo, Justo Lorenzo"],["dc.contributor.author","Ahmadi, Rezvan"],["dc.date.accessioned","2022-04-29T14:53:09Z"],["dc.date.available","2022-04-29T14:53:09Z"],["dc.date.issued","2011-03"],["dc.description.abstract","To study the clinical relevance of undifferentiated tumour cells in astrocytic gliomas we employed a large tumour tissue microarray (n=283) with corresponding clinical data and analyzed the expression of Nestin and Sox-2, which mark undifferentiated stem- and progenitor cells in the normal brain. Both markers were expressed abundantly and staining of nestin significantly increased with WHO grade. Further, nestin and Sox-2 immunoreactivity was significantly associated with tumour cell proliferation and nestin expression was independently associated with poor patient survival. Our findings suggest that immature glioma cells are involved in tumour growth and tumour progression and significantly impact on patient prognosis."],["dc.identifier.doi","10.3109/1354750X.2010.536256"],["dc.identifier.pmid","21323603"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/107110"],["dc.language.iso","en"],["dc.relation.eissn","1366-5804"],["dc.relation.issn","1354-750X"],["dc.title","Association of stem cell-related markers and survival in astrocytic gliomas"],["dc.type","journal_article"],["dc.type.internalPublication","no"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2951"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Clinical Cancer Research"],["dc.bibliographiccitation.lastpage","2962"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Dettling, Steffen"],["dc.contributor.author","Stamova, Slava"],["dc.contributor.author","Warta, Rolf"],["dc.contributor.author","Schnölzer, Martina"],["dc.contributor.author","Rapp, Carmen"],["dc.contributor.author","Rathinasamy, Anchana"],["dc.contributor.author","Reuss, David"],["dc.contributor.author","Pocha, Kolja"],["dc.contributor.author","Roesch, Saskia"],["dc.contributor.author","Jungk, Christine"],["dc.contributor.author","Warnken, Uwe"],["dc.contributor.author","Eckstein, Volker"],["dc.contributor.author","Grabe, Niels"],["dc.contributor.author","Schramm, Christoph"],["dc.contributor.author","Weigand, Markus A."],["dc.contributor.author","von Deimling, Andreas"],["dc.contributor.author","Unterberg, Andreas"],["dc.contributor.author","Beckhove, Philipp"],["dc.contributor.author","Herold-Mende, Christel"],["dc.date.accessioned","2022-04-29T14:55:49Z"],["dc.date.available","2022-04-29T14:55:49Z"],["dc.date.issued","2018"],["dc.description.abstract","Purpose: Successful immunotherapies for IDHmut gliomas require better knowledge of T-cell target antigens. Here, we elucidated their antigen repertoire recognized by spontaneous T-cell responses using an unbiased proteomic approach.Experimental Design: Protein fractionations of tissue lysates from IDHmut gliomas (n = 4) were performed. Fractions were tested by IFNγ ELISpot assay for recognition through patients' T cells. Proteins of immunogenic fractions were identified by mass spectrometry and validated by in silico-predicted synthetic long peptides in patients of origin, additional IDHmut glioma patients (n = 16), and healthy donors (n = 13). mRNA and protein expression of immunogenic antigens was analyzed in tumor tissues and IDHmut glioma stem-like cells (GSC). HLA-A 02-restricted T-cell epitopes were functionally determined by short peptides and numbers of antigen-specific T cells by HLA-peptide tetramer analysis.Results: A total of 2,897 proteins were identified in immunogenic tumor fractions. Based on a thorough filter process, 79 proteins were selected as potential T-cell antigens. Twenty-six of these were recognized by the patients' T cells, and five of them (CRKII, CFL1, CNTN1, NME2, and TKT) in up to 56% unrelated IDHmut glioma patients. Most immunogenic tumor-associated antigens (TAA) were expressed in IDHmut gliomas and GSCs, while being almost absent in normal brain tissues. Finally, we identified HLA-A 02-restricted epitopes for CRKII, NME2, and TKT that were recognized by up to 2.82% of antigen-specific peripheral cytotoxic T cells in IDHmut glioma patients.Conclusions: By analyzing the repertoire of T-cell target antigens in IDHmut glioma patients, we identified five novel immunogenic TAAs and confirmed their expression on IDHmut tumors and GSCs. Clin Cancer Res; 24(12); 2951-62. ©2018 AACR."],["dc.identifier.doi","10.1158/1078-0432.CCR-17-1839"],["dc.identifier.pmid","29563135"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/107149"],["dc.language.iso","en"],["dc.relation.eissn","1557-3265"],["dc.relation.issn","1078-0432"],["dc.title","Identification of CRKII, CFL1, CNTN1, NME2, and TKT as Novel and Frequent T-Cell Targets in Human IDH-Mutant Glioma"],["dc.type","journal_article"],["dc.type.internalPublication","no"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]