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Berlin Brandenburg

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  • 1
    Language: English
    In: Cell and Tissue Research, 2015, Vol.359(1), p.225(30)
    Description: Neurogenesis, the generation of new neurons, is deregulated in neural stem cell (NSC)- and progenitor-derived murine models of malignant medulloblastoma and glioma, the most common brain tumors of children and adults, respectively. Molecular characterization of human malignant brain tumors, and in particular brain tumor stem cells (BTSCs), has identified neurodevelopmental transcription factors, microRNAs, and epigenetic factors known to inhibit neuronal and glial differentiation. We are starting to understand how these factors are regulated by the major oncogenic drivers in malignant brain tumors. In this review, we will focus on the molecular switches that block normal neuronal differentiation and induce brain tumor formation. Genetic or pharmacological manipulation of these switches in BTSCs has been shown to restore the ability of tumor cells to differentiate. We will discuss potential brain tumor therapies that will promote differentiation in order to reduce treatment resistance, suppress tumor growth, and prevent recurrence in patients. Keywords Brain * Glioma * Medulloblastoma * Neurogenesis * Neural stem cells
    Keywords: Gliomas – Analysis ; Stem Cells – Analysis ; Brain Tumors – Analysis
    ISSN: 0302-766X
    E-ISSN: 14320878
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  • 2
    Language: English
    In: Cancer Research, 2014, Vol.74(19)
    Keywords: Medical And Health Sciences ; Clinical Medicine ; Cancer And Oncology ; Medicin Och Hälsovetenskap ; Klinisk Medicin ; Cancer Och Onkologi
    ISSN: 0008-5472
    E-ISSN: 15387445
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  • 3
    Language: English
    In: Cancer Research, 07/15/2016, Vol.76(14 Supplement), pp.2688-2688
    Description: Glioma is the most frequent malignant brain tumor in adults. Platelet-derived growth factor (PDGF) signaling is commonly activated in glioma. We have used a retrovirus-driven PDGFB-induced murine glioma model that causes tumors that closely resemble human gliomas of various grades. Knowing that retroviruses have a capacity to induce insertional mutagenesis, we have employed whole genome sequencing to identify potential genes that, together with PDGFB, drive glioma development.
    Keywords: Genomes ; Brain Tumors ; Insertional Mutagenesis ; Platelet-Derived Growth Factor ; Animal Models ; Genetic Screening ; Development ; Glioma ; Retroviridae ; Development & Cell Cycle;
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: CrossRef
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  • 4
    Language: English
    In: Neuro-Oncology, 2014, Vol.16
    Description: BACKGROUND: Tumor recurrence is the main cause of death for children with medulloblastoma, the most common malignant childhood brain tumor. The MYCN oncogene is a poor prognosis marker and is amplified in the molecularly defined SHH and Group 4 subgroups but rarely in WNT and Group 3 subgroups of human medulloblastoma. Recent findings on childhood brain tumor relapse mechanisms suggest spatiotemporal differences within these four subgroups. SOX9 is a transcription factor that is important for glial fate determination in the brain but has also been found to promote tumor metastasization. We previously showed how expression of SOX9 correlates well with human SHH tumors but only few scattered SOX9-positive cells are found in SHH-independent Group 3 and Group 4 human medulloblastoma. METHODS: In order to study recurrence processes experimentally, we used a previously described transgenic Tet-OFF (Glt1-tTA) inducible model of MYCN-driven SHH-independent medulloblastoma (GTML mouse). To recreate metastatic recurrence we further used a Tet-ON (SOX9-rtTA) model that drives MYCN expression from the SOX9 promoter upon doxycycline treatment. RESULTS: By crossing the GTML Tet-OFF model with a Tet-ON transgene we managed to study rare SOX9-positive tumor cells after SOX9-negative tumor cells were first depleted using doxycycline. SOX9-positive GTML cells were tumorigenic and reinitiated distant recurrences over time. The SOX9-positive cells further showed an increased resistance to MYCN-targeted therapies. Relapses showed similar histopathology but presented generally higher levels SOX9 as compared to primary GTML tumors. A similar correlation was found in Group 3 and Group 4 medulloblastoma patients where isolated metastases had consistently higher SOX9 levels as compared to corresponding primary tumors. Finally, we overexpressed SOX9 in normal cerebellar stem cells transduced with mutationally stabilized MYCN-T58A and injected them back into the cerebellum of adult mice. Surprisingly, SOX9-positive MYCN-T58A brain tumors migrated and developed in the forebrain in contrast to the cerebellar stem cells transduced with MYCN-T58A only. CONCLUSIONS: Our findings suggest that increased levels of SOX9 drives migration in MYCN-driven medulloblastoma. Rare SOX9-positive tumor cells show an increased therapy resistance and are alone capable of reinitiating childhood brain tumors. Further characterization of SOX9-positive cells in Group 3 and Group 4 tumors could help us understand what drives metastatic medulloblastoma relapse and could lead to new therapies directed against these particularly serious cell types. SECONDARY CATEGORY: Tumor Biology.
    Keywords: Medical And Health Sciences ; Clinical Medicine ; Cancer And Oncology ; Medicin Och Hälsovetenskap ; Klinisk Medicin ; Cancer Och Onkologi ; Medical And Health Sciences ; Clinical Medicine ; Neurology ; Medicin Och Hälsovetenskap ; Klinisk Medicin ; Neurologi
    ISSN: 1522-8517
    E-ISSN: 15235866
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