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Hematogenous dissemination of glioblastoma multiforme

Carolin MüllerUniversity Medical Center Hamburg-EppendorfJohannes HoltschmidtKlinik für Senologie, Kliniken Essen-Mitte, D-45136 Essen, GermanyMartina AuerInstitute of Human Genetics, Medical University of Graz, A-8010 Graz, AustriaEllen HeitzerInstitute of Human Genetics, Medical University of Graz, A-8010 Graz, AustriaKatrin LamszusUniversity Medical Center Hamburg-EppendorfAlexander SchulteUniversity Medical Center Hamburg-EppendorfJakob MatschkeUniversity Medical Center Hamburg-EppendorfSabine Langer-FreitagInstitute of Human Genetics, Technical University of Munich, D-81675 Munich, GermanyChristin GaschDepartment of Tumor Biology, University Medical Center Hamburg-Eppendorf, D-201246 Hamburg, GermanyMalgorzata StoupiecUniversity Medical Center Hamburg-EppendorfOliver MauermannDepartment of Tumor Biology, University Medical Center Hamburg-Eppendorf, D-201246 Hamburg, GermanySven PeineUniversity Medical Center Hamburg-EppendorfMarkus GlatzelUniversity Medical Center Hamburg-EppendorfMichael R. SpeicherInstitute of Human Genetics, Medical University of Graz, A-8010 Graz, AustriaJochen B. GeiglInstitute of Human Genetics, Medical University of Graz, A-8010 Graz, AustriaManfred WestphalUniversity Medical Center Hamburg-EppendorfKlaus PantelUniversity Medical Center Hamburg-EppendorfSabine RiethdorfUniversity Medical Center Hamburg-Eppendorf

2014en

ABI

Annotatsiya

Glioblastoma multiforme (GBM) is the most frequent and aggressive brain tumor in adults. The dogma that GBM spread is restricted to the brain was challenged by reports on extracranial metastases after organ transplantation from GBM donors. We identified circulating tumor cells (CTCs) in peripheral blood (PB) from 29 of 141 (20.6%) GBM patients by immunostaining of enriched mononuclear cells with antibodies directed against glial fibrillary acidic protein (GFAP). Tumor cell spread was not significantly enhanced by surgical intervention. The tumor nature of GFAP-positive cells was supported by the absence of those cells in healthy volunteers and the presence of tumor-specific aberrations such as EGFR gene amplification and gains and losses in genomic regions of chromosomes 7 and 10. Release of CTCs was associated with EGFR gene amplification, suggesting a growth potential of these cells. We demonstrate that hematogenous GBM spread is an intrinsic feature of GBM biology.

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Identifikatorlar

DOI: 10.1126/scitranslmed.3009095

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