Matching Items (2)
Filtering by
Description
In a 2004 paper, John Nagy raised the possibility of the existence of a hypertumor \emph{i.e.}, a focus of aggressively reproducing parenchyma cells that invade part or all of a tumor. His model used a system of nonlinear ordinary differential equations to find a suitable set of conditions for which these hypertumors exist. Here that model is expanded by transforming it into a system of nonlinear partial differential equations with diffusion, advection, and a free boundary condition to represent a radially symmetric tumor growth. Two strains of parenchymal cells are incorporated; one forming almost the entirety of the tumor while the much more aggressive strain
appears in a smaller region inside of the tumor. Simulations show that if the aggressive strain focuses its efforts on proliferating and does not contribute to angiogenesis signaling when in a hypoxic state, a hypertumor will form. More importantly, this resultant aggressive tumor is paradoxically prone to extinction and hypothesize is the cause of necrosis in many vascularized tumors.
appears in a smaller region inside of the tumor. Simulations show that if the aggressive strain focuses its efforts on proliferating and does not contribute to angiogenesis signaling when in a hypoxic state, a hypertumor will form. More importantly, this resultant aggressive tumor is paradoxically prone to extinction and hypothesize is the cause of necrosis in many vascularized tumors.
ContributorsAlvarez, Roberto L (Author) / Milner, Fabio A (Thesis advisor) / Nagy, John D. (Committee member) / Kuang, Yang (Committee member) / Thieme, Horst (Committee member) / Mahalov, Alex (Committee member) / Smith, Hal (Committee member) / Arizona State University (Publisher)
Created2014
Description
Glioblastoma multiforme is associated with a very low survival rate and is recognized as the most vicious form of intracranial cancer. The Akt gene pathway has three different isoforms, each of which has a different role in the tumors of GBM. Preliminary data suggests that Akt3 may work to decrease tumorigenicity. A produced image that visualizes the subcellular localization of Akt3 led the author to believe that Akt3 may reduce tumorigenicity by decreasing genomic instability caused by the cancer. To explore this, flow cytometry was performed on GBM cell lines with Akt3v1 over-expression, Akt3v2 over-expression, and a control glioma cell line.
ContributorsGhorayeb, Antoine (Author) / Neisewander, Janet (Thesis director) / Diehnelt, Chris (Committee member) / Moussallem, Suzan (Committee member) / Barrett, The Honors College (Contributor) / College of Liberal Arts and Sciences (Contributor)
Created2012-12