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  • 1
    In: Brain, 2017, Vol. 140(3), pp.e17-e17
    Keywords: Medicine;
    ISSN: 0006-8950
    E-ISSN: 1460-2156
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  • 2
    In: Nature Neuroscience, 2015, Vol.19(1), p.20
    Description: There is a growing recognition that gliomas are complex tumors composed of neoplastic and non-neoplastic cells, which each individually contribute to cancer formation, progression and response to treatment. The majority of the non-neoplastic cells are tumor-associated macrophages (TAMs), either of peripheral origin or representing brain-intrinsic microglia, that create a supportive stroma for neoplastic cell expansion and invasion. TAMs are recruited to the glioma environment, have immune functions, and can release a wide array of growth factors and cytokines in response to those factors produced by cancer cells. In this manner, TAMs facilitate tumor proliferation, survival and migration. Through such iterative interactions, a unique tumor ecosystem is established, which offers new opportunities for therapeutic targeting.
    Keywords: Gliomas – Development and Progression ; Glia – Health Aspects ; Immune Response – Observations;
    ISSN: 1097-6256
    E-ISSN: 15461726
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  • 3
    Language: English
    In: Cell, 22 July 2011, Vol.146(2), pp.187-188
    Description: Investigating the family tree of a tumor to identify its cellular origins is a daunting task. now use an elegant lineage tracing technique (MADM) to visualize glioma from its earliest stages. They show that mutations originally induced in neural stem cells lie dormant and only trigger malignant transformation following differentiation into oligodendrocyte precursor cells.
    Keywords: Biology
    ISSN: 0092-8674
    E-ISSN: 1097-4172
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  • 4
    Language: English
    In: PLoS ONE, 2011, Vol.6(9), p.e24454
    Description: Primary glioblastomas are subdivided into several molecular subtypes. There is an ongoing debate over the cell of origin for these tumor types where some suggest a progenitor while others argue for a stem cell origin. Even within the same molecular subgroup, and using lineage tracing in mouse models, different groups have reached different conclusions. We addressed this problem from a combined mathematical modeling and experimental standpoint. We designed a novel mathematical framework to identify the most likely cells of origin of two glioma subtypes. Our mathematical model of the unperturbed in vivo system predicts that if a genetic event contributing to tumor initiation imparts symmetric self-renewing cell division (such as PDGF overexpression), then the cell of origin is a transit amplifier. Otherwise, the initiating mutations arise in stem cells. The mathematical framework was validated with the RCAS/tv-a system of somatic gene transfer in mice. We demonstrated that PDGF-induced gliomas can be derived from GFAP-expressing cells of the subventricular zone or the cortex (reactive astrocytes), thus validating the predictions of our mathematical model. This interdisciplinary approach allowed us to determine the likelihood that individual cell types serve as the cells of origin of gliomas in an unperturbed system.
    Keywords: Research Article ; Computer Science ; Mathematics ; Medicine ; Oncology ; Computer Science ; Mathematics
    E-ISSN: 1932-6203
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  • 5
    Language: English
    In: Cancer Research, 10/01/2018, Vol.78(19 Supplement), pp.B05-B05
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: CrossRef
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  • 6
    Language: English
    In: Neuroscience Letters, 07 November 2014, Vol.583, pp.130-135
    Description: Both brain-resident microglia and peripheral macrophages/monocytes infiltrate into glioma and promote glioma growth. In the present study we analyzed coupling and membrane currents in glioma-associated microglia and macrophages/monocytes and compared this to control and stab wound-associated microglia. Using the knock-in mouse line, we distinguished membrane currents of glioma-associated microglia and macrophages/monocytes in acute brain slices prepared 14–16 days after inoculation of GL261 glioma cells. The current profile of microglia showed inward rectifying currents reminiscent of an intermediate activation state when compared to other disease models or cell culture. Macrophages/monocytes showed a higher specific outward conductance and a significantly lower capacitance indicative of a smaller membrane area than microglia. As controls, we also recorded currents from control microglia and stab wound-associated microglia. Since there are reports of microglial coupling , we injected biocytin into these cells and analyzed for cell coupling after fixing the slices and processed for biocytin labeling with Cy3-conjugated-Streptavidin. Neither control microglia nor glioma-associated microglia and macrophages/monocytes nor stab wound-associated microglia showed any sign of coupling. Moreover, performing qRT-PCR revealed that no connexin43 was detectable on isolated and sorted glioma-associated microglia and macrophages/monocytes, indicating that these cells are not part of a coupled network.
    Keywords: Glioma-Associated Microglia ; Glioma-Associated Macrophages/Monocytes ; Glioma ; Gap Junctions ; Electrophysiology ; Medicine ; Anatomy & Physiology
    ISSN: 0304-3940
    E-ISSN: 1872-7972
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  • 7
    Language: English
    In: Neuroscience Letters, Nov 7, Vol.583, p.130(6)
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.neulet.2014.09.035 Byline: Nadine Richter, Stefan Wendt, Petya B. Georgieva, Dolores Hambardzumyan, Christiane Nolte, Helmut Kettenmann Abstract: * Membrane currents were recorded from glioma-associated microglia and macrophages/monocytes in acute brain slices 14-16 days after inoculation of glioma cells into mouse cortex. * These two cell types differ in their specific outward conductance and specific membrane capacity. * Glioma-associated microglia and macrophages/monocytes as well as control microglia and stab wound-associated microglia were not coupled to any other cell. Author Affiliation: (a) Max Delbrueck Center for Molecular Medicine, Robert Roessle Str. 10, 13125 Berlin, Germany (b) Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, USA Article History: Received 8 August 2014; Revised 16 September 2014; Accepted 17 September 2014
    Keywords: Gliomas
    ISSN: 0304-3940
    Source: Cengage Learning, Inc.
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  • 8
    Language: English
    In: PLoS ONE, 01 January 2013, Vol.8(4), p.e62150
    Description: In glioblastoma high expression of the CD133 gene, also called Prominin1, is associated with poor prognosis. The PDGF-driven proneural group represents a subset of glioblastoma in which CD133 is not overexpressed. Interestingly, this particular subset shows a relatively good prognosis. As with many other tumors, gliobastoma is believed to arise and be maintained by a restricted population of stem-like cancer cells that express the CD133 transmembrane protein. The significance of CD133(+) cells for gliomagenesis is controversial because of conflicting supporting evidence. Contributing to this inconsistency is the fact that the isolation of CD133(+) cells has largely relied on the use of antibodies against ill-defined glycosylated epitopes of CD133. To overcome this problem, we used a knock-in lacZ reporter mouse, Prom1(lacZ/+) , to track Prom1(+) cells in the brain. We found that Prom1 (prominin1, murine CD133 homologue) is expressed by cells that express markers characteristic of the neuronal, glial or vascular lineages. In proneural tumors derived from injection of RCAS-PDGF into the brains of tv-a;Ink4a-Arf(-/-) Prom1(lacZ/+) mice, Prom1(+) cells expressed markers for astrocytes or endothelial cells. Mice co-transplanted with proneural tumor sphere cells and Prom1(+) endothelium had a significantly increased tumor burden and more vascular proliferation (angiogenesis) than those co-transplanted with Prom1(-) endothelium. We also identified specific genes in Prom1(+) endothelium that code for endothelial signaling modulators that were not overexpressed in Prom1(-) endothelium. These factors may support proneural tumor progression and could be potential targets for anti-angiogenic therapy.
    Keywords: Sciences (General)
    E-ISSN: 1932-6203
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  • 9
    Language: English
    In: The Journal of clinical investigation, April 2011, Vol.121(4), pp.1344-8
    Description: Pilocytic astrocytoma (PA) is the most common type of primary brain tumor in children and the second most frequent cancer in childhood. Children with incompletely resected PA represent a clinically challenging patient cohort for whom conventional adjuvant therapies are only moderately effective. This has produced high clinical demand for testing of new molecularly targeted treatments. However, the development of new therapeutics for PA has been hampered by the lack of an adequate in vivo tumor model. Recent studies have identified activation of MAPK signaling, mainly by oncogenic BRAF activation, as a hallmark genetic event in the pathogenesis of human PA. Using in vivo retroviral somatic gene transfer into mouse neural progenitor cells, we have shown here that ectopic expression of the activated BRAF kinase domain is sufficient to induce PA in mice. Further in vitro analyses demonstrated that overexpression of activated BRAF led to increased proliferation of primary mouse astrocytes that could be inhibited by treatment with the kinase inhibitor sorafenib. Our in vivo model for PA shows that the activated BRAF kinase domain is sufficient to induce PA and highlights its role as a potential therapeutic target.
    Keywords: Astrocytoma -- Etiology ; Brain Neoplasms -- Etiology ; Proto-Oncogene Proteins B-Raf -- Genetics
    ISSN: 00219738
    E-ISSN: 1558-8238
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  • 10
    Language: English
    In: Frontiers in Immunology, May 8, 2018
    Description: Glioblastomas (GBMs) are the most common and aggressive primary brain tumors. Due to their malignant growth and invasion into the brain parenchyma coupled with resistance to therapy, GBMs are among the deadliest of all cancers. GBMs are highly heterogeneous at both the molecular and histological levels. Hallmark histological structures include pseudopalisading necrosis and microvascular proliferation. In addition to high levels of intratumoral heterogeneity, GBMs also exhibit high levels of inter-tumoral heterogeneity. The major non-neoplastic cell population in the GBM microenvironment includes cells of the innate immune system called tumor-associated macrophages (TAMs). Correlative data from the literature suggest that molecularly distinct GBM subtypes exhibit differences in their microenvironment. Data from mouse models of GBM suggest that genetic driver mutations can create unique microenvironments. Here, we review the origin, features, and functions of TAMs in distinct GBM subtypes. We also discuss their interactions with other immune cell constituents and discuss prospects of therapeutically targeting TAMs to increase the efficacy of T-cell functions.
    Keywords: Immune Response -- Research ; Gene Mutation -- Research ; Glioblastomas -- Genetic Aspects ; Glioblastomas -- Research
    ISSN: 1664-3224
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