Kooperativer Bibliotheksverbund

Berlin Brandenburg

and
and

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
Type of Medium
Language
Year
  • 1
    Language: English
    In: Upsala Journal of Medical Sciences, 01 May 2012, Vol.117(2), pp.122-131
    Description: Myc proteins are often deregulated in human brain tumors, especially in embryonal tumors that affect children. Many observations have shown how alterations of these pleiotropic Myc transcription factors provide initiation, maintenance, or progression of tumors. This review will focus on the...
    Keywords: Brain Tumors ; Molecular Biology ; Oncogenes ; Pediatrics ; Protein Phosphorylation ; Tumor Biology ; Medicine
    ISSN: 0300-9734
    E-ISSN: 2000-1967
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    Language: English
    In: Cancer Research, 04/15/2011, Vol.71(8 Supplement), pp.3985-3985
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: CrossRef
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 3
    Language: English
    In: Cancer Research, 04/15/2011, Vol.71(8 Supplement), pp.3451-3451
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: CrossRef
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 4
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 5
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 6
    Language: English
    In: Cancer Research, 2013, Vol.73(8)
    Keywords: Medical And Health Sciences ; Medicin Och Hälsovetenskap
    ISSN: 0008-5472
    E-ISSN: 15387445
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 7
    Language: English
    In: Cancer Research, 07/15/2016, Vol.76(14 Supplement), pp.2473-2473
    Description: Misexpression of MYC genes (MYC and MYCN) occurs commonly in medulloblastoma (MB), the most frequent malignant childhood brain tumor. We previously showed that tumors are addicted to MYCN and that MYCN stabilization is required for MB development in mice (Swartling et al, Genes & Dev, 2010; Cancer Cell, 2012). Targeted MYCN suppression completely depleted MYCN-driven MB cells in vivo. Immediate transcriptional changes from such MYCN blockade were found by RNA-Seq and showed similarities to changes that occurred after CDK2 suppression or when inhibiting BET bromodomains. CDK2 and BET inhibitors both inhibited MYC protein expression and effectively induced cell cycle arrest or apoptosis. Compared with either agent alone a sustained combination treatment over 7-10 days displayed synergy and effectively abolished tumor cell proliferation in vitro. The combined treatment further reduced tumor growth in orthotopical MB transplants and significantly prolonged survival as compared to single agent therapy. Our data suggest that dual inhibition of CDK2 and BET Bromodomains could be a novel treatment approach in suppressing medulloblastoma by targeting MYC proteins.
    Keywords: Brain Tumors ; Myc Protein ; Apoptosis ; Data Processing ; Cell Cycle ; Medulloblastoma ; Transcription ; Children ; Cyclin-Dependent Kinase 2 ; Tumor Cells ; Cancer ; Neurobiology;
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: CrossRef
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 8
    Language: English
    In: Cancer research, 01 February 2017, Vol.77(3), pp.802-812
    Description: High-grade glioma (HGG) is a group of primary malignant brain tumors with dismal prognosis. Whereas adult HGG has been studied extensively, childhood HGG, a relatively rare disease, is less well-characterized. Here, we present two novel platelet-derived growth factor (PDGF)-driven mouse models of pediatric supratentorial HGG. Tumors developed from two different cells of origin reminiscent of neural stem cells (NSC) or oligodendrocyte precursor cells (OPC). Cross-species transcriptomics showed that both models are closely related to human pediatric HGG as compared with adult HGG. Furthermore, an NSC-like cell-of-origin enhanced tumor incidence, malignancy, and the ability of mouse glioma cells (GC) to be cultured under stem cell conditions as compared with an OPC-like cell. Functional analyses of cultured GC from these tumors showed that cells of NSC-like origin were more tumorigenic, had a higher rate of self-renewal and proliferation, and were more sensitive to a panel of cancer drugs compared with GC of a more differentiated origin. These two mouse models relevant to human pediatric supratentorial HGG propose an important role of the cell-of-origin for clinicopathologic features of this disease. Cancer Res; 77(3); 802-12. ©2016 AACR.
    Keywords: Glioma -- Pathology ; Neural Stem Cells -- Pathology ; Neurons -- Pathology ; Oligodendroglia -- Pathology ; Supratentorial Neoplasms -- Pathology
    ISSN: 00085472
    E-ISSN: 1538-7445
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 9
    Language: English
    In: Experimental Neurology, Oct, 2014, Vol.260, p.56(13)
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.expneurol.2013.01.027 Byline: Fredrik J. Swartling, Sara Bolin, Joanna J. Phillips, Anders I. Persson Keywords: Brain tumor; Progenitor; Neural stem cell; Glioma; Medulloblastoma; Reprogramming; miRNA Abstract: Brain tumors have frequently been associated with a neural stem cell (NSC) origin and contain stem-like tumor cells, so-called brain tumor stem cells (BTSCs) that share many features with normal NSCs. A stem cell state of BTSCs confers resistance to radiotherapy and treatment with alkylating agents. It is also a hallmark of aggressive brain tumors and is maintained by transcriptional networks that are also active in embryonic stem cells. Advances in reprogramming of somatic cells into induced pluripotent stem (iPS) cells have further identified genes that drive stemness. In this review, we will highlight the possible drivers of stemness in medulloblastoma and glioma, the most frequent types of primary malignant brain cancer in children and adults, respectively. Signals that drive expansion of developmentally defined neural precursor cells are also active in corresponding brain tumors. Transcriptomal subgroups of human medulloblastoma and glioma match features of NSCs but also more restricted progenitors. Lessons from genetically-engineered mouse (GEM) models show that temporally and regionally defined NSCs can give rise to distinct subgroups of medulloblastoma and glioma. We will further discuss how acquisition of stem cell features may drive brain tumorigenesis from a non-NSC origin. Genetic alterations, signaling pathways, and therapy-induced changes in the tumor microenvironment can drive reprogramming networks and induce stemness in brain tumors. Finally, we propose a model where dysregulation of microRNAs (miRNAs) that normally provide barriers against reprogramming plays an integral role in promoting stemness in brain tumors. Article History: Received 25 October 2012; Revised 19 January 2013; Accepted 24 January 2013
    Keywords: Gliomas -- Analysis ; Brain Tumors -- Analysis ; Embryonic Stem Cells -- Analysis
    ISSN: 0014-4886
    Source: Cengage Learning, Inc.
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 10
    Language: English
    In: Acta Neuropathologica, 2017, Vol.134(5), pp.679-689
    Description: Medulloblastoma is the most frequent malignant brain tumor in childhood, but it may also affect infants, adolescents, and young adults. Recent advances in the understanding of the disease have shed light on molecular and clinical heterogeneity, which is now reflected in the updated WHO classification of brain tumors. At the same time, it is well accepted that preclinical research and clinical trials have to be subgroup-specific. Hence, valid models have to be generated specifically for every medulloblastoma subgroup to properly mimic molecular fingerprints, clinical features, and responsiveness to targeted therapies. This review summarizes the availability of experimental medulloblastoma models with a particular focus on how well these models reflect the actual disease subgroup. We further describe technical advantages and disadvantages of the models and finally point out how some models have successfully been used to introduce new drugs and why some medulloblastoma subgroups are extraordinary difficult to model.
    Keywords: Medulloblastoma ; Mouse model ; SHH ; WNT ; Group 3 ; Group 4
    ISSN: 0001-6322
    E-ISSN: 1432-0533
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. Further information can be found on the KOBV privacy pages