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Friday, September 11, 2015
10:00-11:00 a.m.
102 Colburn Lab
Shelly Peyton
Assistant Professor
Barry & Afsaneh Siadat Career Development Faculty Fellow
Chemical Engineering
University of Massachusetts, Amherst
Shelly Peyton is the Barry and Afsaneh Siadat Assistant Professor of Chemical Engineering at the University of Massachusetts,
Amherst. She received her B.S. in Chemical Engineering from Northwestern University in 2002 and went on to obtain her MS and
PhD in Chemical Engineering from the University of California, Irvine. She was then an NIH Kirschstein post-doctoral fellow in the
Biological Engineering department at MIT before starting her academic appointment at UMass in 2011. Her research interests
are in biomaterial design and understanding how cell-material interactions contribute to cancer aggressiveness, cardiovascular
disease progression, and regenerative medicine. Since arriving at UMass she has been named a Pew Biomedical Scholar, received
a New Innovator Award from the NIH, and she was recently awarded a CAREER grant from the NSF.
Synthetic Environments to Understand Cancer
Metastasis and Drug Resistance
Metastasis is the leading cause of fatality for women diagnosed with breast cancer. The most common
anatomical sites of distant tumor growth include the brain, lung, liver, and bone, and it is well known that this
metastatic spread in breast cancer is not random. Rather, different clinical subtypes of breast cancer exhibit
unique patterns of metastatic site preference, called tissue tropism. Given the physical and chemical diversity of
these secondary tissue sites, my lab hypothesizes that there is a relationship between the biophysical and
biochemical properties of the tissue, and the ability of cells within a particular subtype of breast cancer to adhere,
migrate, grow, and respond to chemotherapeutics at these secondary sites. We created biomaterial
microenvironments, which capture some of the key physical and biochemical elements of the secondary site
tissues often recipient of breast cancer spread (brain, lung, and bone). Our approach is revealing how cellmaterial interactions are predictive of metastatic spread and non-canonical signaling pathways involved in drug
resistance at these tissue sites. First, we can use a cell-ECM screening method in vitro to predict where a cell will
metastasize in vivo (Barney et al. 2015). Second, we have demonstrated that a stiff tumor microenvironment
reduces sorafenib treatment efficacy, which can be abrogated via JNK inhibition (Nguyen et al 2014). We will
discuss these and current efforts toward biomaterial capture of dormant metastatic cells, rapid tumor spheroid
formation, and the role of mesenchymal stem cells in drug resistance. We propose that these types of biomaterial
environments can be used to predict tissue-specific metastasis, and may serve as a system that pharmaceutical
companies can use to rule out false positives and potentially save billions of dollars in the drug development
pipeline.