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SUNMONTUEWEDTHUFRISAT
Events for August 24, 2012
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EE Placement Exams
Fri, Aug 24, 2012 @ 08:00 AM - 11:30 AM
Ming Hsieh Department of Electrical and Computer Engineering
University Calendar
EE 450/EE 479 8:00AM-9:00 AM
EE 457/EE 464/EE 465 9:20 AM-10:20 AM
EE 441/EE477 10:40 AM-11:30 AM
For 400 Level course waiversLocation: Mark Taper Hall Of Humanities (THH) - 101
Audiences: Everyone Is Invited
Contact: Samantha Chew
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USC Physical Sciences in Oncology Monthly Seminar Series
Fri, Aug 24, 2012 @ 11:45 AM - 01:00 PM
Alfred E. Mann Department of Biomedical Engineering
Conferences, Lectures, & Seminars
Speaker: Jeffrey Varner, Associate Professor, Chemical and Biomolecular Engineering, Cornell University
Talk Title: Modeling and Analysis of the Core Architecture Regulating TGFβ Induced Epithelial to Mesenchymal Transition (EMT)
Abstract: The epithelial to mesenchymal transition (EMT) is important in development and pathological processes such as fibrosis and cancer. Transforming growth factor β (TGFβ) initiates EMT, repressing the expression of epithelial genes such E-cadherin, while simultaneously activating the expression of mesenchymal genes such as Vimentin. In this study, we developed a first-generation ordinary differential equation (ODE) model of TGFβ induced EMT. The model contained 80 genes, 995 protein or mRNA components interconnected through 1700 interactions. A family of 15,000 likely model parameter sets (1700 kinetic constants and 56 non-zero initial conditions) was estimated using 41 data sets generated in DLD1 colon carcinoma, MDCKII and A375 melanoma cells using the Pareto optimal ensemble technique (POETs) multiobjective optimization algorithm. Analysis of the model population suggested three important regulatory axes controlled TGFβ induced EMT. First, the AP1 and SP1 transcription factors played differential roles during EMT induction. Deletion of AP1 enhanced E-cadherin expression, while decreasing Vimentin expression. On the other hand, SP1 deletion enhanced Vimentin expression with little or no effect on E-cadherin. Second, overexpression of ERK-specific phosphatases increased the level of phosphorylated Smad2, which enhanced the transition to a mesenchymal phenotype (instead of the expected epithelial phenotype). Lastly, the abundance of LEF1 was a key factor regulating the shift to a mesenchymal phenotype. Taken together, these results provided insight into the core molecular architecture of TGFβ induced EMT, and revealed possible operational paradigms of phenotypic conversion.
Biography: Jeffrey Varner holds a Bachelor of Science degree (Chemistry), a Masters and a Ph.D. degree in Chemical Engineering, all from Purdue University. Prof. Varner's graduate thesis work at Purdue was done under the direction of Prof. D. Ramkrishna in the area of modeling and analysis of metabolic networks. Following Purdue, Prof. Varner was a postdoctoral researcher in the Department of Biology at the ETH-Zurich where he studied signal transduction mechanisms involved in cell-death under Prof. Jay Bailey. After the ETH, Prof. Varner was a Scientist in the Oncology business unit of Genencor International Inc, Palo Alto, CA. While at Genencor, Prof. Varner was involved in the discovery of novel targets in human cancers, and was a project team member for preclinical, phase-I and II studies of protein therapeutics for the treatment of colorectal cancer and Chronic Lymphocytic Leukemia (CLL). Prof. Varner left Genencor at the end of 2005 to join the faculty of the Chemical and Biomolecular Engineering department at Cornell University. At Cornell, the Varner lab is developing physiochemical modeling tools to rationally reprogram human signal transduction architectures.
Host: USC Phyiscal Sciences in Oncology Center
Location: Clinical Science Center (CSC) - Harkness Auditorium #250
Audiences: Everyone Is Invited
Contact: Kristina Gerber
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Welcome Orientation
Fri, Aug 24, 2012 @ 12:00 PM - 01:30 PM
Ming Hsieh Department of Electrical and Computer Engineering
University Calendar
Lunch provided after at EEB
Location: Mark Taper Hall Of Humanities (THH) - 101
Audiences: Everyone Is Invited
Contact: Samantha Chew
