A mathematical model for the onset of avascular tumor growth in response to the loss of p53 function

dc.contributor.author Levine, Howard
dc.contributor.author Smiley, Michael
dc.contributor.author Tucker, Anna
dc.contributor.author Nilsen-Hamilton, Marit
dc.contributor.author Nilsen-Hamilton, Marit
dc.contributor.department Biochemistry, Biophysics and Molecular Biology
dc.contributor.department Mathematics
dc.date 2018-02-17T10:58:03.000
dc.date.accessioned 2020-06-29T23:47:08Z
dc.date.available 2020-06-29T23:47:08Z
dc.date.copyright Sun Jan 01 00:00:00 UTC 2006
dc.date.issued 2006-01-01
dc.description.abstract <p>We present a mathematical model for the formation of an avascular tumor based on the loss by gene mutation of the tumor suppressor function of p53. The wild type p53 protein regulates apoptosis, cell expression of growth factor and matrix metalloproteinase, which are regulatory functions that many mutant p53 proteins do not possess. The focus is on a description of cell movement as the transport of cell population density rather than as the movement of individual cells. In contrast to earlier works on solid tumor growth, a model is proposed for the initiation of tumor growth. The central idea, taken from the mathematical theory of dynamical systems, is to view the loss of p53 function in a few cells as a small instability in a rest state for an appropriate system of differential equations describing cell movement. This instability is shown (numerically) to lead to a second, spatially inhomogeneous, solution that can be thought of as a solid tumor whose growth is nutrient diffusion limited. In this formulation, one is led to a system of nine partial differential equations. We show computationally that there can be tumor states that coexist with benign states and that are highly unstable in the sense that a slight increase in tumor size results in the tumor occupying the sample region while a slight decrease in tumor size results in its ultimate disappearance.</p>
dc.description.comments <p>This is an article from <em>Cancer Informatics</em> 2 (2006): 163. Posted with permission.</p>
dc.format.mimetype application/pdf
dc.identifier archive/lib.dr.iastate.edu/bbmb_ag_pubs/38/
dc.identifier.articleid 1052
dc.identifier.contextkey 8035638
dc.identifier.s3bucket isulib-bepress-aws-west
dc.identifier.submissionpath bbmb_ag_pubs/38
dc.identifier.uri https://dr.lib.iastate.edu/handle/20.500.12876/10768
dc.language.iso en
dc.source.bitstream archive/lib.dr.iastate.edu/bbmb_ag_pubs/38/2006_Nilsen_MathematicalModel.pdf|||Fri Jan 14 23:52:19 UTC 2022
dc.subject.disciplines Biochemistry, Biophysics, and Structural Biology
dc.subject.disciplines Other Mathematics
dc.title A mathematical model for the onset of avascular tumor growth in response to the loss of p53 function
dc.type article
dc.type.genre article
dspace.entity.type Publication
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