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Elizabeth Scribner

Researcher at University of Alabama at Birmingham

Publications -  7
Citations -  106

Elizabeth Scribner is an academic researcher from University of Alabama at Birmingham. The author has contributed to research in topics: Glioma & Estimation theory. The author has an hindex of 5, co-authored 7 publications receiving 98 citations. Previous affiliations of Elizabeth Scribner include University of Alabama.

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

TL;DR: A clinical-scale model of GBM is constructed whose predictions uncover a new pattern of recurrence in 11/70 bevacizumab-treated patients and 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.
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Computational Trials: Unraveling Motility Phenotypes, Progression Patterns, and Treatment Options for Glioblastoma Multiforme

TL;DR: A mathematical model of glioblastoma multiforme growth and invasion in humans and computational trials using agents that target angiogenesis, tumor replication rates, or motility are applied and a correlation was observed between the efficacy of the rate-reducing agent and the prolongation of overall survival times.
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Single Cell Mathematical Model Successfully Replicates Key Features of GBM: Go-Or-Grow Is Not Necessary.

TL;DR: It is suggested that the GoG phenotype is not a necessary property for the formation of the multilayer structure, recurrence patterns, and the poor survival times of patients diagnosed with GBM.
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Proper orthogonal decomposition for parameter estimation in oscillating biological networks

TL;DR: The findings reveal that POD generates accurate estimates of the parameters even in the presence of experimental noise; furthermore, extrapolating biologically measured data points to a number of oscillations improves the curve fits, C^1 approximations, and parameter estimations.
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Key rates for the grades and transformation ability of glioma: model simulations and clinical cases.

TL;DR: The hypothesis that constant rates of dispersion, proliferation, and angiogenesis prescribe either a natural evolution or the inability to progress to higher grades is supported.