We study mechanisms of cancer progression, using principles of tissue and organ development. Pattern formation and morphogenesis have traditionally been considered the preserves of developmental biology and distal to the theory of carcinogenesis since neoplastic transformation has been shown to entail loss of tissue architecture and patterning. This conceptualization is being revised by efforts that show that as cancer progression can also lead cellular reorganization and patterning during invasion. 

 

Such reorganization is not without its inherent principles and constraints. We focus on discovering these organizational principles and how they influence cancer phenotype, metastasis, and outcome. To study these problems, we investigate the dynamics of extracellular matrix (ECM: laminins and collagens), glycocalyx-glycans (sialic acids), and lectins (galectins), all of which are critical to the construction of the tissue homeostasis but are dysregulated in cancer dissemination.

 

We employ experimental approaches within the contexts of breast and ovarian cancer metastasis, as well as theoretical efforts using simulations and bioinformatics towards building experimentally motivated frameworks to understand their multiscale dynamics. A multidisciplinary approach encompassing inputs from physical sciences and engineering are not just insightful, but essential to study morphogenesis in pathological contexts. Our experimental results help propose cancer invasion as a tractable model of an excitable biological system capable of cellular organization.