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• W2113128467 startingPage "e115018" @default.
• W2113128467 abstract "Glioblastoma 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." @default.
• W2113128467 created "2016-06-24" @default.
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• W2113128467 date "2014-12-15" @default.
• W2113128467 modified "2023-09-25" @default.
• W2113128467 title "Effects of Anti-Angiogenesis on Glioblastoma Growth and Migration: Model to Clinical Predictions" @default.
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• W2113128467 doi "https://doi.org/10.1371/journal.pone.0115018" @default.
• W2113128467 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4266618" @default.
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• W2113128467 hasPublicationYear "2014" @default.
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