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020 ▼a 9780438091528
035 ▼a (MiAaPQ)AAI10871374
035 ▼a (MiAaPQ)OhioLINK:osu1492739871307445
040 ▼a MiAaPQ ▼c MiAaPQ ▼d 247004
0820 ▼a 610
1001 ▼a Volakis, Leonithas Ioannis.
24510 ▼a Evaluating Dynamic Changes in Cancer Cell Mechanics during Epithelial to Mesenchymal Transition.
260 ▼a [S.l.]: ▼b The Ohio State University., ▼c 2017.
260 1 ▼a Ann Arbor: ▼b ProQuest Dissertations & Theses, ▼c 2017.
300 ▼a 191 p.
500 ▼a Source: Dissertation Abstracts International, Volume: 79-10(E), Section: B.
500 ▼a Adviser: Samir Ghadiali.
5021 ▼a Thesis (Ph.D.)--The Ohio State University, 2017.
520 ▼a Cancer metastasis is a major cause of mortality, with Epithelial-to-Mesenchymal Transition (EMT) playing a role in facilitating increased invasion and motility. During metastasis, epithelial cells detach from the primary tumor and may acquire a
520 ▼a Currently, there is limited information about how the tumor's mechanical and biophysical properties influence EMT and metastasis. In Chapter 2, we address these knowledge gaps. Major findings for Chapter 2 include: (1) EMT progression using TGF-
520 ▼a Following the canonical model, TGF-beta induced EMT in pancreatic cancer cells (Panc1) and non-cancer keratinocytes (HACAT) was evaluated. Major findings for Chapter 3 include: (1) In both models biomechanical features can assess EMT progression
520 ▼a Results from Chapters 2 and 3 suggest that altering tumor mechanics is a viable way to mitigate the initial stages of metastasis, and cell adhesion and stiffness represent the robust biomechanical features during EMT progression. Chapter 4 build
590 ▼a School code: 0168.
650 4 ▼a Biomedical engineering.
690 ▼a 0541
71020 ▼a The Ohio State University. ▼b Biomedical Engineering.
7730 ▼t Dissertation Abstracts International ▼g 79-10B(E).
773 ▼t Dissertation Abstract International
790 ▼a 0168
791 ▼a Ph.D.
792 ▼a 2017
793 ▼a English
85640 ▼u http://www.riss.kr/pdu/ddodLink.do?id=T15000220 ▼n KERIS ▼z 이 자료의 원문은 한국교육학술정보원에서 제공합니다.
980 ▼a 201812 ▼f 2019
990 ▼a ***1012033