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      Genomic Analysis of the BMP Family in Glioblastomas

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          Abstract

          Glioblastoma multiforme (GBM) is a grade IV glioma with a median survival of 15 months. Recently, bone morphogenetic protein (BMP) signaling has been shown to promote survival in xenograft murine models. To gain a better understanding of the role of BMP signaling in human GBMs, we examined the genomic alterations of 90 genes associated with BMP signaling in GBM patient samples. We completed this analysis using publically available datasets compiled through The Cancer Genome Atlas and the Glioma Molecular Diagnostic Initiative. Here we show how mRNA expression is altered in GBM samples and how that is associated with patient survival, highlighting both known and novel associations between BMP signaling and GBM biology.

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          Molecular subclasses of high-grade glioma predict prognosis, delineate a pattern of disease progression, and resemble stages in neurogenesis.

          Heidi Phillips, Samir Kharbanda, Ruihuan Chen … (2006)
          Previously undescribed prognostic subclasses of high-grade astrocytoma are identified and discovered to resemble stages in neurogenesis. One tumor class displaying neuronal lineage markers shows longer survival, while two tumor classes enriched for neural stem cell markers display equally short survival. Poor prognosis subclasses exhibit markers either of proliferation or of angiogenesis and mesenchyme. Upon recurrence, tumors frequently shift toward the mesenchymal subclass. Chromosomal locations of genes distinguishing tumor subclass parallel DNA copy number differences between subclasses. Functional relevance of tumor subtype molecular signatures is suggested by the ability of cell line signatures to predict neurosphere growth. A robust two-gene prognostic model utilizing PTEN and DLL3 expression suggests that Akt and Notch signaling are hallmarks of poor prognosis versus better prognosis gliomas, respectively.
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            Bone morphogenetic proteins inhibit the tumorigenic potential of human brain tumour-initiating cells.

            S G M Piccirillo, B A Reynolds, N Zanetti … (2006)
            Transformed, oncogenic precursors, possessing both defining neural-stem-cell properties and the ability to initiate intracerebral tumours, have been identified in human brain cancers. Here we report that bone morphogenetic proteins (BMPs), amongst which BMP4 elicits the strongest effect, trigger a significant reduction in the stem-like, tumour-initiating precursors of human glioblastomas (GBMs). Transient in vitro exposure to BMP4 abolishes the capacity of transplanted GBM cells to establish intracerebral GBMs. Most importantly, in vivo delivery of BMP4 effectively blocks the tumour growth and associated mortality that occur in 100% of mice after intracerebral grafting of human GBM cells. We demonstrate that BMPs activate their cognate receptors (BMPRs) and trigger the Smad signalling cascade in cells isolated from human glioblastomas (GBMs). This is followed by a reduction in proliferation, and increased expression of markers of neural differentiation, with no effect on cell viability. The concomitant reduction in clonogenic ability, in the size of the CD133+ population and in the growth kinetics of GBM cells indicates that BMP4 reduces the tumour-initiating cell pool of GBMs. These findings show that the BMP-BMPR signalling system--which controls the activity of normal brain stem cells--may also act as a key inhibitory regulator of tumour-initiating, stem-like cells from GBMs and the results also identify BMP4 as a novel, non-cytotoxic therapeutic effector, which may be used to prevent growth and recurrence of GBMs in humans.
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              Rembrandt: helping personalized medicine become a reality through integrative translational research.

              Subha Madhavan, Jean-Claude Zenklusen, Yuri Kotliarov … (2009)
              Finding better therapies for the treatment of brain tumors is hampered by the lack of consistently obtained molecular data in a large sample set and the ability to integrate biomedical data from disparate sources enabling translation of therapies from bench to bedside. Hence, a critical factor in the advancement of biomedical research and clinical translation is the ease with which data can be integrated, redistributed, and analyzed both within and across functional domains. Novel biomedical informatics infrastructure and tools are essential for developing individualized patient treatment based on the specific genomic signatures in each patient's tumor. Here, we present Repository of Molecular Brain Neoplasia Data (Rembrandt), a cancer clinical genomics database and a Web-based data mining and analysis platform aimed at facilitating discovery by connecting the dots between clinical information and genomic characterization data. To date, Rembrandt contains data generated through the Glioma Molecular Diagnostic Initiative from 874 glioma specimens comprising approximately 566 gene expression arrays, 834 copy number arrays, and 13,472 clinical phenotype data points. Data can be queried and visualized for a selected gene across all data platforms or for multiple genes in a selected platform. Additionally, gene sets can be limited to clinically important annotations including secreted, kinase, membrane, and known gene-anomaly pairs to facilitate the discovery of novel biomarkers and therapeutic targets. We believe that Rembrandt represents a prototype of how high-throughput genomic and clinical data can be integrated in a way that will allow expeditious and efficient translation of laboratory discoveries to the clinic.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Transl Oncogenomics
                Journal ID (iso-abbrev): Transl Oncogenomics
                Journal ID (publisher-id): Translational Oncogenomics
                Title: Translational Oncogenomics
                Publisher: Libertas Academica
                ISSN (Electronic): 1177-2727
                Publication date Collection: 2015
                Publication date (Electronic): 15 April 2015
                Volume: 7
                Pages: 1-9
                Affiliations
                [1 ]Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, TN, USA.
                [2 ]Department of Cancer Biology, Vanderbilt University Medical Center, Nashville, TN, USA.
                Author notes
                Article
                Publisher ID: tog-7-2015-001
                DOI: 10.4137/TOG.S22256
                PMC ID: 4406393
                PubMed ID: 25987829
                SO-VID: e4cdf7d9-e959-49f2-b183-c659537dbf05
                Copyright © © 2015 the author(s), publisher and licensee Libertas Academica Ltd.
                License:

                This is an open-access article distributed under the terms of the Creative Commons CCCC-BY-NCNC 3.0 License.

                History
                Date received : 26 November 2014
                Date revision received : 22 January 2015
                Date accepted : 29 January 2015
                Categories
                Subject: Original Research

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: glioblastoma multiforme,bone morphogenetic protein,genomics,the cancer genome atlas,rembrandt
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: glioblastoma multiforme, bone morphogenetic protein, genomics, the cancer genome atlas, rembrandt

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