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  • 1
    Language: English
    In: Neuroimmunology and Neuroinflammation, 2014, Vol.1(1), p.6
    Description: 〈b〉Journal Title in English: 〈/b〉Neuroimmunology and Neuroinflammation
    Keywords: Immune Response – Genetic Aspects ; Microglia – Genetic Aspects ; Central Nervous System Diseases – Development and Progression ; Central Nervous System Diseases – Genetic Aspects
    ISSN: 2347-8659
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  • 2
    In: PLoS ONE, 2013, Vol.8(6)
    Description: Natural Killer Gene Complex (NKC)–encoded C-type lectin-like receptors (CTLRs) are expressed on various immune cells including T cells, NK cells and myeloid cells and thereby contribute to the orchestration of cellular immune responses. Some NKC-encoded CTLRs are grouped into the C-type lectin family 2 (CLEC2 family) and interact with genetically linked CTLRs of the NKRP1 family. While many CLEC2 family members are expressed by hematopoietic cells (e.g. CD69 ( CLEC2C) ), others such as the keratinocyte-associated KACL ( CLEC2A ) are specifically expressed by other tissues. Here we provide the first characterization of the orphan gene CLEC2L . In contrast to other CLEC2 family members, CLEC2L is conserved among mammals and located outside of the NKC. We show that CLEC2L -encoded CTLRs are expressed as non-glycosylated, disulfide-linked homodimers at the cell surface. CLEC2L expression is fairly tissue-restricted with a predominant expression in the brain. Thus CLEC2L -encoded CTLRs were designated BACL (brain-associated C-type lectin). Combining in situ hybridization and immunohistochemistry, we show that BACL is expressed by neurons in the CNS, with a pronounced expression by Purkinje cells. Notably, the CLEC2L locus is adjacent to another orphan CTLR gene ( KLRG2 ), but reporter cell assays did neither indicate interaction of BACL with the KLRG2 ectodomain nor with human NK cell lines or lymphocytes. Along these lines, growth of BACL-expressing tumor cell lines in immunocompetent mice did not provide evidence for an immune-related function of BACL. Altogether, the CLEC2L gene encodes a homodimeric cell surface CTLR that stands out among CLEC2 family members by its conservation in mammals, its biochemical properties and the predominant expression in the brain. Future studies will have to reveal insights into the functional relevance of BACL in the context of its neuronal expression.
    Keywords: Research Article ; Biology
    E-ISSN: 1932-6203
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  • 3
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States, Sept 3, 2013, Vol.110(36), p.14735(6)
    Description: Disruption of the blood--brain barrier (BBB) is a hallmark of acute inflammatory lesions in multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis. This disruption may precede and facilitate the infiltration of encephalitogenic T cells. The signaling events that lead to this BBB disruption are incompletely understood but appear to involve dysregulation of tight-junction proteins such as claudins. Pharmacological interventions aiming at stabilizing the BBB in MS might have therapeutic potential. Here, we show that the orally available small molecule LY-317615, a synthetic bisindolylmaleimide and inhibitor of protein kinase C[beta], which is clinically under investigation for the treatment of cancer, suppresses the transmigration of activated T cells through an inflamed endothelial cell barrier, where it leads to the induction of the tight-junction molecules zona occludens-1, claudin 3, and claudin 5 and other pathways critically involved in transendothelial leukocyte migration. Treatment of mice with ongoing experimental autoimmune encephalomyelitis with LY-317615 ameliorates inflammation, demyelination, axonal damage, and clinical symptoms. Although LY-317615 dose-dependently suppresses T-cell proliferation and cytokine production independent of antigen specificity, its therapeutic effect is abrogated in a mouse model requiring pertussis toxin. This abrogation indicates that the anti-inflammatory and clinical efficacy is mainly mediated by stabilization of the BBB, thus suppressing the transmigration of encephalitogenic T cells. Collectively, our data suggest the involvement of endothelial protein kinase C[beta] in stabilizing the BBB in autoimmune neuroinflammation and imply a therapeutic potential of BBB-targeting agents such as LY-317615 as therapeutic approaches for MS. EAE | enzastaurin | CNS www.pnas.org/cgi/doi/10.1073/pnas.1302569110
    Keywords: Protein Kinases -- Physiological Aspects ; Protein Kinases -- Health Aspects ; Blood-brain Barrier -- Physiological Aspects ; Blood-brain Barrier -- Health Aspects ; Encephalomyelitis -- Physiological Aspects
    ISSN: 0027-8424
    Source: Cengage Learning, Inc.
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  • 4
    Language: English
    In: PLoS ONE, 01 January 2015, Vol.10(5), p.e0127123
    Description: Current pathological diagnostics include the analysis of (epi-)genetic alterations as well as oncogenic pathways. Deregulated mammalian target of rapamycin complex 1 (mTORC1) signaling has been implicated in a variety of cancers including malignant gliomas and is considered a promising target in cancer treatment. Monitoring of mTORC1 activity before and during inhibitor therapy is essential. The aim of our study is to provide a recommendation and report on pitfalls in the use of phospho-specific antibodies against mTORC1-targets phospho-RPS6 (Ser235/236; Ser240/244) and phospho-4EBP1 (Thr37/46) in formalin fixed, paraffin embedded material.Primary, established cell lines and brain tumor tissue from routine diagnostics were assessed by immunocyto-, immunohistochemistry, immunofluorescent stainings and immunoblotting. For validation of results, immunoblotting experiments were performed. mTORC-pathway activation was pharmacologically inhibited by torin2 and rapamycin. Torin2 treatment led to a strong reduction of signal intensity and frequency of all tested antibodies. In contrast phospho-4EBP1 did not show considerable reduction in staining intensity after rapamycin treatment, while immunocytochemistry with both phospho-RPS6-specific antibodies showed a reduced signal compared to controls. Staining intensity of both phospho-RPS6-specific antibodies did not show considerable decrease in stability in a timeline from 0-230 minutes without tissue fixation, however we observed a strong decrease of staining intensity in phospho-4EBP1 after 30 minutes. Detection of phospho-signals was strongly dependent on tissue size and fixation gradient. mTORC1-signaling was significantly induced in glioblastomas although not restricted to cancer cells but also detectable in non-neoplastic cells.Here we provide a recommendation for phospho-specific immunohistochemistry for patient-orientated therapy decisions and monitoring treatment response.
    Keywords: Sciences (General)
    E-ISSN: 1932-6203
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  • 5
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  • 6
    Language: English
    In: Anti-Cancer Agents in Medicinal Chemistry, 2010, Vol.10(6), p.438-449
    Description: Induction of caspase-dependent apoptosis (type I cell death) is a major mechanism by which most chemotherapeutic drugs and radiation kill tumor cells. However, conventional cancer therapies fail to mediate their effects in a target-specific fashion. The extremely unfavorable prognosis for patients suffering from glioblastomas (GBMs) is strongly correlated to the intrinsic apoptosis resistance of GBM cells which especially occurs in diffusely migrating tumor cells. The ultimate goal for molecular, apoptosis-based therapies is to target specific components of the two major apoptotic pathways, i.e. the extrinsic and the intrinsic pathway to trigger tumor-selective apoptosis, while at the same time limiting toxicity in normal tissues. Induction of autophagic cell death (type II cell death) by proautophagic drugs is an alternative and emerging concept to trigger glioma cell death and to exploit caspase-independent programmed cell death pathways for the development of novel glioma therapies. This review provides an up to date and comprehensive report on the relevant pre-clinical and clinical drugs interfering with the major apoptosis and autophagy pathways, their therapeutic potential in glioma and adresses potential future perspectives in this exciting field of research.
    Keywords: Apoptosis ; Autophagy ; Death Receptor ; Caspase ; Bcl-2 ; Inhibitor Of Apoptosis ; Mtor ; Akt ; Lysosomal Protease ; Beclin1 ; Glioblastoma ; Caspase-Dependent Apoptosis ; Tumor Cells ; Autophagic Cell Death ; Cancer ; Apaf-1 ; Caspase Recruitment Domain ; Programmed Cell Death ; Autophagosomes ; Malignant Gliomas ; Apoptotic Peptidase Activating Factor 1 ; Cytochrome C ; Tuberous Sclerosis 1 ; Pi3 Kinase ; Tumor Necrosis Factor ; Deathinducing Signaling Complex ; Antineoplastic Agents ; Temozolomide ; Proteasome Inhibitors ; Histone Deacetylase Inhibitors ; Mammalian Target Of Rapamycin ; Iap Inhibitors ; Mithramycin A ; Anti-Xiap Therapy ; Adenine Nucleotide Translocator-1 ; Mitochondrial Permeability Pore ; Bcl-2 Homology Domains ; Bcl-2-Homolgy Domain-3 ; Abt-263 ; Abt-737 ; Bcl-2 Antisense Oligonucleotide ; Chronic Lymphocytic Leukemia ; Cyt997 ; Atg6/Beclin1 ; Pyruvate Dehydrogenase Kinase ; Growth Hormone-Releasing Hormone ; Phosphatidylinositol 3-Kinase ; Rapamycin ; Temsirolimus ; Perifosine ; Xl765 ; Microtubule-Associated Proteins ; Tetrahydrocannabinol ; P53 ; Nutlins ; Cns Neoplasms
    ISSN: 1871-5206
    E-ISSN: 1875-5992
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  • 7
    Language: English
    In: Current Medical Imaging Reviews, 2010, Vol.6(4), p.200-219
    Description: The 4th edition of the WHO (World Health Organization) classification of tumours of the central nervous system published in 2007 provides several new entities, new variants of established entities as well as changes in the tumour grading system. In addition, new molecular markers are introduced and information about the genetic bases of brain tumour development is extended. This review gives an overview about the current WHO classification system, discusses remaining controversies and provides an introduction of the standard diagnostic procedures.
    Keywords: Cns ; Brain ; Spinal Cord ; Who Classification ; Central Nervous System ; Tnm Classification ; Hematoxylin ; Eosin ; Neuroectodermal Origin ; Choroid Plexus ; Pineal Neoplasms ; Astrocytic Tumours ; Pilocytic Astrocytomas ; Eosinophilic Granular Bodies ; Egbs ; Glial Fibrillary Acidic Protein ; Gfap ; Pilomyxoid Astrocytoma ; Pleomorphic Xanthoastrocytomas ; Pxas ; Diffusely Infiltrating Astrocytomas ; Anaplastic Astrocytomas ; Glioblastoma ; Small Cell Glioblastoma ; Giant Cell Glioblastoma ; Gliomatosis Cerebri ; Oligodendroglioma ; Mixed Glial Neoplasms ; Subependymoma ; Myxopapillary Ependymoma ; Ependymomas ; Anaplastic Ependymoma ; Atypical Choroid Plexus Papilloma ; Choroid Plexus Papilloma ; Astroblastoma ; Chordoid Glioma ; Angiocentric Glioma ; Dysplastic Gangliocytomas ; Lhermitte-Duclos Disease ; Desmoplastic Infantile Astrocytoma ; Dia ; Ganglioglioma ; Dig ; Dysembryoplastic Neuroepithelial Tumour ; Gangliogliomas ; Gangliocytomas ; Central Neurocytoma ; Extraventricular Neurocytoma ; Cerebellar Liponeurocytoma ; Spinal Paraganglioma ; Papillary Glioneuronal Tumour ; Pineoblastoma ; Papillary Tumour ; Medulloblastoma ; Primitive Neuroectodermal Tumours ; Medulloepithelioma ; Ependymoblastoma ; Atypical Teratoid/Rhabdoid Tumour ; At/Rt ; Schwannomas ; Neurofibromas ; Perineurioma ; Malignant Peripheral Nerve Sheath Tumour ; Mpnst ; Meningiomas ; Haemangioblastoma ; Haemangiopericytoma ; Melanocytoma ; Malignant Melanoma ; Craniopharyngioma ; Granular Cell Tumour (Gct) ; Spindle Cell Oncocytoma ; Sco
    ISSN: 1573-4056
    E-ISSN: 1875-6603
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  • 8
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States of America, 09 September 2014, Vol.111(36), pp.E3775-84
    Description: Pre-B-cell leukemia homeobox (Pbx)-regulating protein-1 (Prep1) is a ubiquitous homeoprotein involved in early development, genomic stability, insulin sensitivity, and hematopoiesis. Previously we have shown that Prep1 is a haploinsufficient tumor suppressor that inhibits neoplastic transformation by competing with myeloid ecotropic integration site 1 for binding to the common heterodimeric partner Pbx1. Epithelial-mesenchymal transition (EMT) is controlled by complex networks of proinvasive transcription factors responsive to paracrine factors such as TGF-β. Here we show that, in addition to inhibiting primary tumor growth, PREP1 is a novel EMT inducer and prometastatic transcription factor. In human non-small cell lung cancer (NSCLC) cells, PREP1 overexpression is sufficient to trigger EMT, whereas PREP1 down-regulation inhibits the induction of EMT in response to TGF-β. PREP1 modulates the cellular sensitivity to TGF-β by inducing the small mothers against decapentaplegic homolog 3 (SMAD3) nuclear translocation through mechanisms dependent, at least in part, on PREP1-mediated transactivation of a regulatory element in the SMAD3 first intron. Along with the stabilization and accumulation of PBX1, PREP1 induces the expression of multiple activator protein 1 components including the proinvasive Fos-related antigen 1 (FRA-1) oncoprotein. Both FRA-1 and PBX1 are required for the mesenchymal changes triggered by PREP1 in lung tumor cells. Finally, we show that the PREP1-induced mesenchymal transformation correlates with significantly increased lung colonization by cells overexpressing PREP1. Accordingly, we have detected PREP1 accumulation in a large number of human brain metastases of various solid tumors, including NSCLC. These findings point to a novel role of the PREP1 homeoprotein in the control of the TGF-β pathway, EMT, and metastasis in NSCLC.
    Keywords: Ptgfβ ; Tale Proteins ; Epithelial-Mesenchymal Transition ; Signal Transduction ; Adenocarcinoma -- Pathology ; Carcinoma, Non-Small-Cell Lung -- Pathology ; Homeodomain Proteins -- Metabolism ; Lung Neoplasms -- Pathology ; Smad3 Protein -- Metabolism ; Transforming Growth Factor Beta -- Metabolism
    ISSN: 00278424
    E-ISSN: 1091-6490
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  • 9
    Language: English
    In: Cancer Research, 04/15/2012, Vol.72(8 Supplement), pp.3401-3401
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: CrossRef
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  • 10
    Language: English
    In: Cancer Research, 01/01/2015, Vol.75(1 Supplement), pp.B70-B70
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: CrossRef
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