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Effects of Anti-Angiogenesis on Glioblastoma Growth and Migration: Model to Clinical Predictions

hal.structure.identifierDepartment of Mathematics [Birmingham, Alabama]
dc.contributor.authorSCRIBNER, Elizabeth
hal.structure.identifierModélisation, contrôle et calcul [MC2]
dc.contributor.authorSAUT, Olivier
hal.structure.identifierDepartment of neurology [Birmingham, Alabama]
dc.contributor.authorPAULA, Province
hal.structure.identifierDepartment of Radiology [Birmingham, Alabama]
dc.contributor.authorASIM, Bag
hal.structure.identifierModélisation, contrôle et calcul [MC2]
dc.contributor.authorCOLIN, Thierry
hal.structure.identifierDepartment of neurology [Birmingham, Alabama]
hal.structure.identifierDepartment of Mathematics [Birmingham, Alabama]
dc.contributor.authorFATHALLAH, Hassan
dc.date.created2014-08-27
dc.date.issued2014-12-15
dc.identifier.issn1932-6203
dc.description.abstractEnGlioblastoma multiforme (GBM) causes significant neurological morbidity and short survival times. Brain invasion by GBM is associated with poor prognosis. Recent clinical trials of bevacizumab in newly-diagnosed GBM found no beneficial effects on overall survival times; however, the baseline health-related quality of life and performance status were maintained longer in the bevacizumab group and the glucocorticoid requirement was lower. Here, we construct a clinical-scale model of GBM whose predictions uncover a new pattern of recurrence in 11/70 bevacizumab-treated patients. The findings support an exception to the Folkman hypothesis: GBM grows in the absence of angiogenesis by a cycle of proliferation and brain invasion that expands necrosis. Furthermore, necrosis is positively correlated with brain invasion in 26 newly-diagnosed GBM. The unintuitive results explain the unusual clinical effects of bevacizumab and suggest new hypotheses on the dynamic clinical effects of migration by active transport, a mechanism of hypoxia-driven brain invasion.
dc.language.isoen
dc.publisherPublic Library of Science
dc.title.enEffects of Anti-Angiogenesis on Glioblastoma Growth and Migration: Model to Clinical Predictions
dc.typeArticle de revue
dc.identifier.doi10.1371/journal.pone.0115018
dc.subject.halMathématiques [math]/Analyse numérique [math.NA]
bordeaux.journalPLoS ONE
bordeaux.page21
bordeaux.peerReviewedoui
hal.identifierhal-01101651
hal.version1
hal.origin.linkhttps://hal.archives-ouvertes.fr//hal-01101651v1
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