Effects of Anti-Angiogenesis on Glioblastoma Growth and Migration: Model to Clinical Predictions
FATHALLAH, Hassan
Department of neurology [Birmingham, Alabama]
Department of Mathematics [Birmingham, Alabama]
< Réduire
Department of neurology [Birmingham, Alabama]
Department of Mathematics [Birmingham, Alabama]
Langue
en
Article de revue
Ce document a été publié dans
PLoS ONE. 2014-12-15p. 21
Public Library of Science
Résumé en anglais
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 ...Lire la suite >
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.< Réduire
Origine
Importé de halUnités de recherche