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Berlin Brandenburg

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  • 1
    In: Neuro-Oncology, 2017, Vol. 19(11), pp.1427-1428
    Keywords: Medicine;
    ISSN: 1522-8517
    E-ISSN: 1523-5866
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  • 2
    Language: English
    In: PLoS ONE, 2011, Vol.6(5), p.e19823
    Description: 1-methyl-D-tryptophan (1-D-MT) is currently being used in clinical trials in patients with relapsed or refractory solid tumors with the aim of inhibiting indoleamine-2,3-dioxygenase (IDO)-mediated tumor immune escape. IDO is expressed in tumors and tumor-draining lymph nodes and degrades tryptophan (trp) to create an immunsuppressive micromilieu both by depleting trp and by accumulating immunosuppressive metabolites of the kynurenine (kyn) pathway. Here we show that proliferation of alloreactive T-cells cocultured with IDO1-positive human cancer cells paradoxically was inhibited by 1-D-MT. Surprisingly incubation with 1-D-MT increased kyn production of human cancer cells. Cell-free assays revealed that 1-D-MT did not alter IDO1 enzymatic activity. Instead, 1-D-MT induced IDO1 mRNA and protein expression through pathways involving p38 MAPK and JNK signalling. Treatment of cancer patients with 1-D-MT has transcriptional effects that may promote rather than suppress anti-tumor immune escape by increasing IDO1 in the cancer cells. These off-target effects should be carefully analyzed in the ongoing clinical trials with 1-D-MT.
    Keywords: Research Article ; Biology ; Chemistry ; Medicine ; Immunology ; Chemistry ; Molecular Biology ; Oncology ; Pharmacology ; Biochemistry
    E-ISSN: 1932-6203
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  • 3
    Language: English
    In: 2012, Vol.7(10), p.e47663
    Description: Enhancer of zeste homolog 2 (EZH2) is the catalytic subunit of the Polycomb-repressive complex 2 (PRC2) that epigenetically silences gene transcription through histone H3 lysine trimethylation (H3K27me3). EZH2 has been implicated in stem cell maintenance and is overexpressed in hematological and solid malignancie`s including malignant glioma. EZH2 is thought to promote tumor progression by silencing tumor suppressor genes. Hence pharmacological disruption of the PRC2 is an attractive therapeutic strategy for cancer treatment. Here we show that EZH2 is expressed in human glioma and correlates with malignancy. Silencing of EZH2 reduced glioma cell proliferation and invasiveness. While we did not observe induction of cell cycle-associated tumor suppressor genes by silencing or pharmacological inhibition of EZH2, microarray analyses demonstrated a strong transcriptional reduction of the AXL receptor kinase. Neither histone nor DNA methylation appeared to be involved in the positive regulation of AXL by EZH2. Silencing AXL mimicked the antiinvasive effects of EZH2 knockdown. Finally, AXL expression is found in human gliomas with high EZH2 expression. Collectively these data suggest that EZH2 drives glioma invasiveness via transcriptional control of AXL independent of histone or DNA methylation.
    Keywords: Research Article ; Biology ; Medicine ; Genetics And Genomics ; Molecular Biology ; Computational Biology ; Oncology
    E-ISSN: 1932-6203
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  • 4
    Article
    Article
    In: Neuro-Oncology, 2018, Vol. 20(12), pp.1561-1562
    Keywords: Meningioma -- Genetics ; Telomerase -- Genetics;
    ISSN: 1522-8517
    E-ISSN: 1523-5866
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  • 5
    Language: English
    In: Acta Neuropathologica, 2015, Vol.129(1), pp.155-155
    Keywords: Astrocytoma -- Classification ; Brain Neoplasms -- Classification ; Oligodendroglioma -- Classification;
    ISSN: 0001-6322
    E-ISSN: 1432-0533
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  • 6
    Language: English
    In: PLoS ONE, 01 January 2013, Vol.8(3), p.e57924
    Description: OBJECTIVES: The application of susceptibility weighted imaging (SWI) in brain tumor imaging is mainly used to assess tumor-related "susceptibility based signals" (SBS). The origin of SBS in glioblastoma is still unknown, potentially representing calcifications or blood depositions. Reliable...
    Keywords: Sciences (General)
    E-ISSN: 1932-6203
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  • 7
    In: Journal Of The National Cancer Institute, 2017, Vol. 109(3), pp.1-4
    Description: High-throughput analyses have revealed the presence of activating mutations in the AKT1 gene in a subpopulation of meningiomas. We report a female patient with multiple intracranial tumor manifestations and histologically verified meningotheliomatous meningioma in the lung. The tumor was continuously growing at multiple sites despite six surgical resections, radiotherapy, and two lines of systemic therapy. Following detection of an AKT1 E17K mutation in three independent tumor samples by sequencing, treatment with AZD5363, a selective AKT inhibitor, was initiated. Ex vivo cultured meningioma cells exhibited sensitivity to the drug as shown by pAKT accumulation on immunoblots. Treatment with AZD5363 resulted, for the first time, in stable disease and minor radiographic response. The patient has been on that treatment for more than one year with ongoing clinical and radiographic response. This is the first report of an AKT1-mutant meningioma responding to AKT inhibition, suggesting that molecular screening may result in clinical benefit.
    Keywords: Cancer Metastasis – Analysis ; Meningioma – Care and Treatment ; Gene Mutation – Research ; Gene Therapy – Analysis;
    ISSN: 0027-8874
    E-ISSN: 1460-2105
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  • 8
    Language: English
    In: Archives of neurology, April 2012, Vol.69(4), pp.523-6
    Description: To analyze infiltration patterns of IDH1 mutant diffuse gliomas into the brain by identification of single tumor cells applying an antibody specific to mutant IDH1 R132H protein. Immunohistochemical analysis. University hospital. Whole-brain and hemisphere sections of 4 patients diagnosed with diffuse glioma. Tumor cells were identified in areas that appeared inconspicuous macroscopically and at histological analysis with respect to cellularity, cellular pleomorphism, or mitotic activity in all cases. Detection of single tumor cells throughout the brain demonstrates diffuse glioma to represent systemic brain disease.
    Keywords: Brain Neoplasms -- Genetics ; Glioma -- Genetics ; Isocitrate Dehydrogenase -- Genetics ; Mutation -- Genetics
    ISSN: 00039942
    E-ISSN: 1538-3687
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  • 9
    Language: English
    In: The Journal of clinical investigation, February 2015, Vol.125(2), pp.593-606
    Description: For a targeted cancer vaccine to be effective, the antigen of interest needs to be naturally processed and presented on MHC by the target cell or an antigen-presenting cell (APC) in the tumor stroma. The presence of these characteristics is often assumed based on animal models, evaluation of antigen-overexpressing APCs in vitro, or assays of material-consuming immune precipitation from fresh solid tissue. Here, we evaluated the use of an alternative approach that uses the proximity ligation assay (PLA) to identify the presentation of an MHC class II-restricted antigen in paraffin-embedded tissue sections from patients with brain tumors. This approach required a specific antibody directed against the epitope that was presented. We used an antibody that specifically binds an epitope of mutated isocitrate dehydrogenase type 1 (IDH1R132H), which is frequently expressed in gliomas and other types of tumors. In situ PLA showed that the IDH1R132H epitope colocalizes with MHC class II in IDH1R132H-mutated glioma tissue. Moreover, PLA demonstrated colocalization between the class II epitope-containing melanoma antigen New York esophageal 1 and MHC class II. Collectively, our data suggest that PLA may be a useful tool to acquire information on whether an antigen is presented in situ, and this technique has potential to guide clinical studies that use antigen-specific cancer immunotherapy.
    Keywords: Antigen Presentation ; Mutation, Missense ; Antigen-Presenting Cells -- Immunology ; Brain Neoplasms -- Immunology ; Glioma -- Immunology ; Immunohistochemistry -- Methods ; Isocitrate Dehydrogenase -- Immunology
    ISSN: 00219738
    E-ISSN: 1558-8238
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  • 10
    Language: English
    In: Clinical cancer research : an official journal of the American Association for Cancer Research, 01 January 2012, Vol.18(1), pp.105-17
    Description: Recent work points out a role of B7H3, a member of the B7-family of costimulatory proteins, in conveying immunosuppression and enforced invasiveness in a variety of tumor entities. Glioblastoma is armed with effective immunosuppressive properties resulting in an impaired recognition and ineffective attack of tumor cells by the immune system. In addition, extensive and diffuse invasion of tumor cells into the surrounding brain tissue limits the efficacy of local therapies. Here, 4IgB7H3 is assessed as diagnostic and therapeutic target for glioblastoma. To characterize B7H3 in glioblastoma, we conduct analyses not only in glioma cell lines and glioma-initiating cells but also in human glioma tissue specimens. B7H3 expression by tumor and endothelial cells correlates with the grade of malignancy in gliomas and with poor survival. Both soluble 4IgB7H3 in the supernatant of glioma cells and cell-bound 4IgB7H3 are functional and suppress natural killer cell-mediated tumor cell lysis. Gene silencing showed that membrane and soluble 4IgB7H3 convey a proinvasive phenotype in glioma cells and glioma-initiating cells in vitro. These proinvasive and immunosuppressive properties were confirmed in vivo by xenografted 4IgB7H3 gene silenced glioma-initiating cells, which invaded significantly less into the surrounding brain tissue in an orthotopic model and by subcutaneously injected LN-229 cells, which were more susceptible to natural killer cell-mediated cytotoxicity than unsilenced control cells. Because of its immunosuppressive and proinvasive function, 4IgB7H3 may serve as a therapeutic target in the treatment of glioblastoma.
    Keywords: B7 Antigens -- Metabolism ; Cell Movement -- Immunology ; Cytotoxicity, Immunologic -- Immunology ; Glioblastoma -- Immunology ; Killer Cells, Natural -- Immunology
    ISSN: 1078-0432
    E-ISSN: 15573265
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