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  • Monographic component part  (383)
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  • 1
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    Noninvasive positron emission tomography and fluorescence imaging of CD133+ tumor stem cells (2014)
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    UID:
    (DE-627)148513689X
    Format: 10
    ISSN: 1091-6490
    Note: Gesehen am 07.10.2014
    In: National Academy of Sciences (Washington, DC), Proceedings of the National Academy of Sciences of the United States of America, Washington, DC : National Acad. of Sciences, 1915, 111(2014), 6, Seite E692-E701, 1091-6490
    In: volume:111
    In: year:2014
    In: number:6
    In: pages:E692-E701
    In: extent:10
    Language: English
    DOI: 10.1073/pnas.1314189111
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  • 2
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    Antigenic expression and spontaneous immune responses support the use of a selected peptide set from the IMA950 glioblastoma vaccine for immunotherapy of grade II and III glioma (2018)
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    UID:
    (DE-627)158208209X
    Format: 11
    ISSN: 2162-402X
    Content: Gliomas are lethal brain tumors that resist standard therapeutic approaches. Immunotherapy is a promising alternative strategy mostly developed in the context of glioblastoma. However, there is a need for implementing immunotherapy for grade II/III gliomas, as these are the most common CNS tumors in young adults with a high propensity for recurrence, making them lethal despite current treatments. We recently identified HLA-A2-restricted tumor-associated antigens by peptide elution from glioblastoma and formulated a multipeptide vaccine (IMA950) evaluated in phase I/II clinical trials with promising results. Here, we investigated expression of the IMA950 antigens in patients with grade II/III astrocytoma, oligodendroglioma or ependymoma, at the mRNA, protein and peptide levels. We report that the BCAN, CSPG4, IGF2BP3, PTPRZ1 and TNC proteins are significantly over-expressed at the mRNA (n = 159) and protein (n = 36) levels in grade II/III glioma patients as compared to non-tumor samples (IGF2BP3 being absent from oligodendroglioma). Most importantly, we detected spontaneous antigen-specific T cell responses to one or more of the IMA950 antigens in 100% and 71% of grade II and grade III patients, respectively (27 patients tested). These patients displayed T cell responses of better quality (higher frequency, broader epitope targeting) than patients with glioblastoma. Detection of spontaneous T cell responses to the IMA950 antigens shows that these antigens are relevant for tumor targeting, which will be best achieved by combination with CD4 epitopes such as the IDH1R132H peptide. Altogether, we provide the rationale for using a selective set of IMA950 peptides for vaccination of patients with grade II/III glioma.
    Note: Gesehen am 18.10.2018 , Published online: 07 Nov 2017
    In: OncoImmunology, Abingdon : Taylor & Franics, 2012, 7(2018), 2, Artikel-ID 1391972, 2162-402X
    In: volume:7
    In: year:2018
    In: number:2
    In: elocationid:1391972
    In: extent:11
    Language: English
    DOI: 10.1080/2162402X.2017.1391972
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  • 3
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    Microenvironment and brain tumor stem cell maintenance : impact of the niche (2014)
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    UID:
    (DE-627)1733701702
    Format: 10
    ISSN: 1875-5992
    Content: There is a lot of experimental evidence that brain tumors might be sustained by a subpopulation of immature cells, so-called brain tumor stem cells (BTSCs), which do not only drive tumor formation but are highly resistant to conventional therapies. Recent findings suggest a critical role of the molecular and cellular tumor microenvironment in which these cells reside for the maintenance of stem cell properties and therapy resistance. However, detection of different BTSC phenotypes even in the same patient tumor and the observation of a marked plasticity due to instability of the BTSC phenotype caused by the environmental niche have led to a controversial discussion on the validity of the cancer stem cell concept. What complicates the situation even more is that there are different types of niches and little is known about the interplay of the niche components with one another and with different types of BTSCs in the context of stem cell maintenance. In this article we review our current knowledge on different BTSC phenotypes and the cellular components and physiology of the niche in which these cells reside. In addition, we will summarize the molecular and functional interaction of niche cells and niche conditions and how this impacts on BTSC maintenance.
    Note: Gesehen am 24.09.2020
    In: Anti-cancer agents in medicinal chemistry, Sharjah : Bentham Sc. Publ., 2006, 14(2014), 8, Seite 1065-1074, 1875-5992
    In: volume:14
    In: year:2014
    In: number:8
    In: pages:1065-1074
    In: extent:10
    Language: English
    DOI: 10.2174/1871520614666140825103636
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  • 4
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    Mutant IDH1 differently affects redox state and metabolism in glial cells of normal and tumor origin (16)
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    UID:
    (DE-627)1690462094
    Format: 20
    ISSN: 2072-6694
    Content: IDH1R132H (isocitrate dehydrogenase 1) mutations play a key role in the development of low-grade gliomas. IDH1wt converts isocitrate to α-ketoglutarate while reducing nicotinamide adenine dinucleotide phosphate (NADP+), whereas IDH1R132H uses α-ketoglutarate and NADPH to generate the oncometabolite 2-hydroxyglutarate (2-HG). While the effects of 2-HG have been the subject of intense research, the 2-HG independent effects of IDH1R132H are still ambiguous. The present study demonstrates that IDH1R132H expression but not 2-HG alone leads to significantly decreased tricarboxylic acid (TCA) cycle metabolites, reduced proliferation, and enhanced sensitivity to irradiation in both glioblastoma cells and astrocytes in vitro. Glioblastoma cells, but not astrocytes, showed decreased NADPH and NAD+ levels upon IDH1R132H transduction. However, in astrocytes IDH1R132H led to elevated expression of the NAD-synthesizing enzyme nicotinamide phosphoribosyltransferase (NAMPT). These effects were not 2-HG mediated. This suggests that IDH1R132H cells utilize NAD+ to restore NADP pools, which only astrocytes could compensate via induction of NAMPT. We found that the expression of NAMPT is lower in patient-derived IDH1-mutant glioma cells and xenografts compared to IDH1-wildtype models. The Cancer Genome Atlas (TCGA) data analysis confirmed lower NAMPT expression in IDH1-mutant versus IDH1-wildtype gliomas. We show that the IDH1 mutation directly affects the energy homeostasis and redox state in a cell-type dependent manner. Targeting the impairments in metabolism and redox state might open up new avenues for treating IDH1-mutant gliomas.
    Note: Gesehen am 20.02.2020
    In: Cancers, Basel : MDPI, 2009, 11(2019,12) Artikel-Nummer 2028, 20 Seiten, 2072-6694
    In: volume:11
    In: year:2019
    In: number:12
    In: extent:20
    Language: English
    DOI: 10.3390/cancers11122028
    URL: Volltext
    URL: https://www.mdpi.com/2072-6694/11/12/2028
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  • 5
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    Helping EGFR inhibition to block cancer (26)
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    UID:
    (DE-627)1584589779
    Format: 3
    ISSN: 1546-1726
    Content: Effectiveness of EGFR treatment is impaired through an early adaptive response. TNF-JNK-Axl-ERK signaling contributes to this primary resistance to EGFR inhibition and might serve as novel target to improve EGFR inhibition.
    Note: Gesehen am 28.11.2018
    In: Nature neuroscience, New York, NY : Nature America, 1998, 20(2017), 8, Seite 1035-1037, 1546-1726
    In: volume:20
    In: year:2017
    In: number:8
    In: pages:1035-1037
    In: extent:3
    Language: English
    DOI: 10.1038/nn.4605
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  • 6
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    Stem cell-associated heterogeneity in Glioblastoma results from intrinsic tumor plasticity shaped by the microenvironment (16)
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    UID:
    (DE-627)1665343591
    Format: 16
    ISSN: 2041-1723
    Content: Cancer stem cells (CSCs) comprise a putative population that can drive growth and resistance. Here, in glioblastoma models the authors show that rather than being a distinct clonal entity, the CSC population represents a plastic state adoptable by most cancer cells via reversible state transitions induced by the microenvironment.
    Note: Gesehen am 14.05.2019
    In: Nature Communications, [London] : Nature Publishing Group UK, 2010, 10(2019) Artikel-Nummer 1787, 16 Seiten, 2041-1723
    In: volume:10
    In: year:2019
    In: pages:1-16
    In: extent:16
    Language: English
    DOI: 10.1038/s41467-019-09853-z
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  • 7
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    Gliosarcoma is driven by alterations in PI3K/Akt, RAS/MAPK pathways and characterized by collagen gene expression signature (27)
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    UID:
    (DE-627)1679978659
    Format: 18
    ISSN: 2072-6694
    Content: Gliosarcoma is a very rare brain tumor reported to be a variant of glioblastoma (GBM), IDH-wildtype. While differences in molecular and histological features between gliosarcoma and GBM were reported, detailed information on the genetic background of this tumor is lacking. We intend to fill in this knowledge gap by the complex analysis of somatic mutations, indels, copy number variations, translocations and gene expression patterns in gliosarcomas. Using next generation sequencing, we determined somatic mutations, copy number variations (CNVs) and translocations in 10 gliosarcomas. Six tumors have been further subjected to RNA sequencing analysis and gene expression patterns have been compared to those of GBMs. We demonstrate that gliosarcoma bears somatic alterations in gene coding for PI3K/Akt (PTEN, PI3K) and RAS/MAPK (NF1, BRAF) signaling pathways that are crucial for tumor growth. Interestingly, the frequency of PTEN alterations in gliosarcomas was much higher than in GBMs. Aberrations of PTEN were the most frequent and occurred in 70% of samples. We identified genes differentially expressed in gliosarcoma compared to GBM (including collagen signature) and confirmed a difference in the protein level by immunohistochemistry. We found several novel translocations (including translocations in the RABGEF1 gene) creating potentially unfavorable combinations. Collected results on genetic alterations and transcriptomic profiles offer new insights into gliosarcoma pathobiology, highlight differences in gliosarcoma and GBM genetic backgrounds and point out to distinct molecular cues for targeted treatment.
    Note: Gesehen am 25.10.2019
    In: Cancers, Basel : MDPI, 2009, 11(2019,3) Artikel-Nummer 284, 18 Seiten, 2072-6694
    In: volume:11
    In: year:2019
    In: number:3
    In: pages:284
    In: extent:18
    Language: English
    DOI: 10.3390/cancers11030284
    URL: Volltext
    URL: https://www.mdpi.com/2072-6694/11/3/284
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  • 8
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    Insight into the complex regulation of CD133 in glioma (2011)
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    UID:
    (DE-627)1807894657
    Format: 10
    ISSN: 1097-0215
    Content: The transmembrane protein CD133 and its extracellular epitope AC133 are controversial cancer markers. In glioma, AC133 demarcates a subpopulation of stem-like tumor cells, so-called cancer stem cells (CSCs), which seem to drive tumor formation and are highly resistant to conventional chemo- and radiotherapy. Lately, experimental evidence for the existence of AC133-independent CSCs has challenged the importance previously attributed to AC133-positive glioma cells. These findings either imply that (i) AC133-positive and AC133-negative glioma cells comprise different, independent CSC populations, (ii) AC133-positive glioma cells are derived from primordial AC133-negative CSCs or (iii) AC133-negative CSCs have lost AC133 expression, while retaining their stem-like features and tumor initiation capacity, and can reacquire AC133 expression in vivo. In our article, we review evidence for and against each of the possible tumor models in glioma and will discuss technical hurdles in the AC133 detection process. In addition, we will outline new insights into CD133 regulation, which suggest certain degree of plasticity between some AC133-positive and AC133-negative CSC populations.
    Note: Online 17 Sep2010 , Gesehen am 27.06.2022
    In: International journal of cancer, Bognor Regis : Wiley-Liss, 1966, 128(2011), 3, Seite 501-510, 1097-0215
    In: volume:128
    In: year:2011
    In: number:3
    In: pages:501-510
    In: extent:10
    Language: English
    DOI: 10.1002/ijc.25687
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  • 9
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    Non-invasive glioblastoma immunoprofiling by printed peptide arrays (26)
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    UID:
    (DE-627)1724278010
    Format: 3
    ISSN: 2162-402X
    Content: Immune monitoring assays for patient stratification and treatment efficacy in clinical trials are in demand. We have recently described a cost-effective non-invasive assay to determine the immune status of glioblastoma patients. Profiling antitumor serum antibodies by customized printed peptide arrays identified response against a tenascin-C (TNC) peptide as a robust prognostic biomarker.
    Note: Gesehen am 10.07.2020
    In: OncoImmunology, Abingdon : Taylor & Franics, 2012, 5(2016,2) Artikel-Nummer e106994, 3 Seiten, 2162-402X
    In: volume:5
    In: year:2016
    In: number:2
    In: extent:3
    Language: English
    DOI: 10.1080/2162402X.2015.1069941
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  • 10
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    Glutathione peroxidase 1 activity dictates the sensitivity of glioblastoma cells to oxidative stress (01)
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    UID:
    (DE-627)1577506995
    Format: 16
    ISSN: 1098-1136
    Content: The high intratumoral and intertumoral heterogeneity of glioblastoma (GBM) leads to resistance to different therapies, and hence, selecting an effective therapy is very challenging. We hypothesized that the antioxidant enzyme status is a significant feature of GBM heterogeneity. The most important reactive oxygen/nitrogen species (ROS/RNS) detoxification mechanisms include superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx). Expression and activity of these enzymes and the cellular response to induced oxidative stress were systematically analyzed and compared between GBM cells and nontransformed glial cells of both human and murine origin. Regardless of cell type or species, all tested cells expressed similar amount of catalase and MnSOD. All except one, GBM cell lines exhibited a deficiency in GPx1 expression and activity. Analysis of GBM tissue sections indicated a heterogeneous profile of weak to moderate expression of GPx1 in tumor cells. GPx1 deficiency led to an accumulation of ROS/RNS and subsequent death of GBM cells after induction of oxidative stress. Astrocytes, microglia/macrophages, and glioma stem cell lines expressed active GPx1 and resisted ROS/RNS-mediated cell death. Pharmacological inhibition or siRNA silencing of GPx1 partially reverted this resistance in astrocytes, indicating the contribution of various antioxidant molecules besides GPx1. The GPx1-expressing GBM cell line on the contrary, became extremely sensitive to oxidative stress after GPx1 inhibition. Altogether, these results highlight GPx1 as a crucial element over other antioxidant enzymes for oxidative stress regulation in GBM cells. Mapping the antioxidant enzyme status of GBM may prove to be a useful tool for personalized ROS/RNS inducing therapies. © 2012 Wiley Periodicals, Inc.
    Note: Gesehen am 11.07.2018
    In: Glia, Bognor Regis [u.a.] : Wiley-Liss, 1988, 60(2012), 11, Seite 1785-1800, 1098-1136
    In: volume:60
    In: year:2012
    In: number:11
    In: pages:1785-1800
    In: extent:16
    Language: English
    DOI: 10.1002/glia.22397
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