DOI

10.17077/etd.d741ter4

Document Type

Thesis

Date of Degree

Spring 2016

Access Restrictions

Access restricted until 07/03/2019

Degree Name

MS (Master of Science)

Degree In

Biomedical Engineering

First Advisor

Michael D. Henry

Second Advisor

Sarah Celeste Vigmostad

First Committee Member

James A. Ankrum

Abstract

Cancer cells traveling to distant tissues during metastasis must survive passing through the circulation. However, the influence of this fluid microenvironment on these cells is poorly understood. It was previously viewed that exposure to the hemodynamic shear forces within circulation was inhospitable to cancer cells, causing the cells to be destroyed. Recent evidence indicates that transformed cells are markedly more resistant to fluid shear stress when compared to non-transformed epithelial cells. Furthermore, these cells selectively adapt following exposure to fluid shear stresses and become more resistant to subsequent exposures to shear stress. The mechanisms behind this difference in phenotype and induced resistance are investigated. The elastic modulus, a measure of stiffness, may play a role in resistance and is shown to be altered upon exposure to fluid shear forces. Additionally, plasma membrane repair is a critical process in the resistance phenotype as cells sustain damage but are able to maintain viability. Cytoskeletal dynamics are also shown to play a role in resistance to fluid shear forces.

Keywords

cancer, fluid shear stress, mechanics, repair, resistance, stiffness

Pages

x, 114 pages

Bibliography

Includes bibliographical references (pages 109-114).

Copyright

Copyright © 2016 Benjamin Lee Krog

Available for download on Wednesday, July 03, 2019

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