The Peyton Lab, Tufts University
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Cancer Bioengineering, Traumatic Brain Injury, Soft Materials, and More
Departments of Biomedical Engineering, Chemical and Biological Engineering, and Graduate School of Biomedical Sciences
Our Research
Why does breast cancer spread to the bone, brain, liver, or lungs, and what lets it survive treatment once it gets there? Our lab tackles questions like these by combining materials engineering with cell biology, building simplified, tunable models of human tissue that let us isolate how specific properties of a cancer cell's environment regulates metastasis, relapse, and drug resistance. We apply the same approach to understanding how the physical forces of traumatic brain injury harm cells in the brain.
How does the ECM Regulate Metastasis and Dormancy?
Metastasis is the leading cause of fatality for women diagnosed with breast cancer. 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 to adhere, migrate, grow, and enter/exit dormancy at these secondary sites. We approach this problem by tuning our biomaterials platforms to capture some of the key physical and biochemical elements of the secondary site tissues often recipient of breast cancer spread (brain, lung, and bone marrow). Our approach has thus far revealed how cell-material interactions are predictive of metastatic spread and how ECM proteins (specifically fibronectin) regulate dormancy of breast cancer in the bone marrow.
Selected Relevant Publications:
Richbourg et al., Science Advances 2024
Barney et al., Science Advances 2020
Kim et al., Advanced Healthcare Materials 2023
Barney et al., Integrative Biology 2015
Edwards, Wagner, and Peyton, Current Opinion in Biomedical Engineering 2026
Building Tissue Mimicking Biomaterials
The vast majority of materials available to study how environmental cues direct cell fate are two-dimensional (2D). In real tissue, cells live surrounded by three-dimensional (3D) ECM, which provides structure and drives cell function. One of the lab’s overarching goals is to create environments (hydrogels from synthetic polymers) that more closely recapitulate this complex tissue environment. My lab designs synthetic polymer hydrogels, which are reproducible, cheap, easy to use, and still mimic structural and physiochemical features of specific in vivo environments. We have published several papers that describe the design of a synthetic, tissue-mimicking hydrogels with tailored and tunable protein composition and biomechanics, which we apply to several complex problems in biology (e.g. cancer metastasis, drug resistance, traumatic brain injury, and more).
Selected Relevant Publications:
Kundu et al., Advanced Materials 2023
Richbourg et al., Advanced Materials 2026
Jansen et al., Biomaterials 2022
Galarza et al., Advanced Healthcare Materials 2020
How does the ECM Regulate Cancer Drug Resistance?
The biomaterials we have built over the years are particularly useful for drug screening applications to make better predictions of efficacy, offering better translation to preclinical models and clinical trials. With these tools, we have revealed how ECM stiffness and geometry impact on how cells sense and respond to chemotherapy and targeted drugs. We have also written commentary on modifying best practices for translating findings from 2D environments to 3D to pre-clinical models. We have collaborated others to solve field-wide issues with inconsistent reporting and improper use of drug response metrics, largely a result of vast differences in cell growth rates across a large variety of biomaterial designs used.
Selected Relevant Publications:
Pritchard, Lee, and Peyton, Soft Matter 2022
Brooks et al., Philosophical Transactions B 2019
What are the physical drivers of cell movement?
Particularly important to cancer metastasis is the ability of cells to migrate in different ECM environments. My lab has studied how the biophysical properties of biomaterials dictate cell motility. This work includes the first report that cell motility on 2D surfaces has a biphasic dependence on ECM stiffness and includes studies of smooth muscle cells, mesenchymal stem cells from bone marrow, osteoblasts, and cancer. We have come to realize that stiffness is just one of many factors controlling this phenotype, and we have designed systems with multifactorial control over stiffness alongside many other biophysical and chemical cues from the matrix. In fact, in certain scenarios (e.g. laminin-rich environments, narrow pore sizes), stiffness does not play a role in dictating motility, at least across the cell types we’ve tested.
Selected Relevant Publications:
Galarza et al., Bioengineering and Translational Medicine 2019
Luzhansky et al., APL Bioengineering 2018
Quantifying and Controlling the Mechanics of Tissues and Materials
Critical for creating the model material systems described above, my lab has developed and adapted a variety of approaches to characterize the mechanical properties (namely modulus and fracture energy) of materials and tissues. These approaches include cavitation rheology, in collaboration with Al Crosby, which can describe the microscale mechanics of tissues in situ, and which we have recently extended to understand how cavitation in brain leads to fracture and traumatic brain injury. Quantification of the modulus and fracture of real tissue feeds back to how we design tissue mimics, and we are now creating next-generation materials that can sense and respond to outside forces (strain-stiffening materials).
Mechanics of Tissues:
Traumatic Brain Injury:
Dougan et al., Biophysical Journal 2024
Dougan et al., Biophysical Journal 2022
Strain-stiffening gels:
Lorenzana et al., Chemistry Letters 2026
Lorenzana et al., Macromolecules 2024
