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dc.contributor.authorVasaikar, Suhas
dc.contributor.authorTsipras, Giorgos
dc.contributor.authorLandázuri, Natalia
dc.contributor.authorCosta, Helena
dc.contributor.authorWilhelmi, Vanessa
dc.contributor.authorScicluna, Patrick
dc.contributor.authorCui, Huanhuan L.
dc.contributor.authorMohammad, Abdul-Aleem
dc.contributor.authorDavoudi, Belghis
dc.contributor.authorShang, Mingmei
dc.contributor.authorAnanthaseshan, Sharan
dc.contributor.authorStrååt, Klas
dc.contributor.authorStragliotto, Giuseppe
dc.contributor.authorRahbar, Afsar
dc.contributor.authorWong, Kum Thong
dc.contributor.authorTegner, Jesper
dc.contributor.authorYaiw, Koon-Chu
dc.contributor.authorSöderberg-Naucler, Cecilia
dc.date.accessioned2018-02-08T13:20:56Z
dc.date.available2018-02-08T13:20:56Z
dc.date.issued2018-02-06
dc.identifier.citationVasaikar S, Tsipras G, Landázuri N, Costa H, Wilhelmi V, et al. (2018) Overexpression of endothelin B receptor in glioblastoma: a prognostic marker and therapeutic target? BMC Cancer 18. Available: http://dx.doi.org/10.1186/s12885-018-4012-7.
dc.identifier.issn1471-2407
dc.identifier.pmid29409474
dc.identifier.doi10.1186/s12885-018-4012-7
dc.identifier.urihttp://hdl.handle.net/10754/627076
dc.description.abstractBackgroundGlioblastoma (GBM) is the most common malignant brain tumor with median survival of 12-15 months. Owing to uncertainty in clinical outcome, additional prognostic marker(s) apart from existing markers are needed. Since overexpression of endothelin B receptor (ETBR) has been demonstrated in gliomas, we aimed to test whether ETBR is a useful prognostic marker in GBM and examine if the clinically available endothelin receptor antagonists (ERA) could be useful in the disease treatment.MethodsData from The Cancer Genome Atlas and the Gene Expression Omnibus database were analyzed to assess ETBR expression. For survival analysis, glioblastoma samples from 25 Swedish patients were immunostained for ETBR, and the findings were correlated with clinical history. The druggability of ETBR was assessed by protein-protein interaction network analysis. ERAs were analyzed for toxicity in in vitro assays with GBM and breast cancer cells.ResultsBy bioinformatics analysis, ETBR was found to be upregulated in glioblastoma patients, and its expression levels were correlated with reduced survival. ETBR interacts with key proteins involved in cancer pathogenesis, suggesting it as a druggable target. In vitro viability assays showed that ERAs may hold promise to treat glioblastoma and breast cancer.ConclusionsETBR is overexpressed in glioblastoma and other cancers and may be a prognostic marker in glioblastoma. ERAs may be useful for treating cancer patients.
dc.description.sponsorshipThis work was supported by Sten A Olssons Foundation for Research and Culture, Family Erling-Persson Foundation, Torsten Söderberg Foundation, BILTEMA Foundation, lngaBritt and Arne Lundbergs Foundation, Stichting af Jochnick Foundation, Jane and Dan Olssons Research Foundation, Nexttobe, Swedish Cancer Foundation, Children’s Cancer Foundation, Swedish Medical Research Council, Thematic Cardiovascular Research Center and Stockholm County Council, and the Swedish Heart-Lung Foundation, VINNOVA-BIO-X and Medivir AB (all to CSN), Cure cancer /Bota Cancer (to KCY). The funding body had no role in the design of the study and collection, analysis, and interpretation of data and in writing the manuscript.
dc.publisherSpringer Nature
dc.relation.urlhttps://bmccancer.biomedcentral.com/articles/10.1186/s12885-018-4012-7
dc.rightsThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectGlioblastoma
dc.subjectEndothelin B receptor
dc.subjectEndothelin receptor antagonists
dc.titleOverexpression of endothelin B receptor in glioblastoma: a prognostic marker and therapeutic target?
dc.typeArticle
dc.contributor.departmentBiological and Environmental Sciences and Engineering (BESE) Division
dc.contributor.departmentBioscience Program
dc.contributor.departmentComputer, Electrical and Mathematical Sciences and Engineering (CEMSE) Division
dc.identifier.journalBMC Cancer
dc.eprint.versionPublisher's Version/PDF
dc.contributor.institutionUnit of Computational Medicine, Center for Molecular Medicine, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
dc.contributor.institutionCell and Molecular Immunology, Experimental Cardiovascular Unit, Departments of Medicine and Neurology, Center for Molecular Medicine, Karolinska Institutet, SE-171 76 Stockholm, Sweden.
dc.contributor.institutionDepartment of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.
dc.contributor.institutionDepartment of Neurosurgery, Karolinska University Hospital, Stockholm, Sweden.
dc.contributor.institutionDepartment of Pathology, University of Malaya, Kuala Lumpur, Malaysia.
kaust.personTegner, Jesper
dc.relation.issupplementedbyDOI:10.6084/m9.figshare.c.3998010.v1
dc.relation.issupplementedbyDOI:10.6084/m9.figshare.5862591.v1
refterms.dateFOA2018-06-13T10:57:47Z
display.relations<b> Is Supplemented By:</b> <br/> <ul> <li><i>[Dataset]</i> <br/> . DOI: <a href="https://doi.org/10.6084/m9.figshare.c.3998010.v1">10.6084/m9.figshare.c.3998010.v1</a> HANDLE: <a href="http://hdl.handle.net/10754/664016">10754/664016</a></li></ul><b> Is Supplemented By:</b> <br/> <ul> <li><i>[Dataset]</i> <br/> . DOI: <a href="https://doi.org/10.6084/m9.figshare.5862591.v1">10.6084/m9.figshare.5862591.v1</a> HANDLE: <a href="http://hdl.handle.net/10754/664017">10754/664017</a></li></ul>
dc.date.published-online2018-02-06
dc.date.published-print2018-12


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This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
Except where otherwise noted, this item's license is described as This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.