What I cannot create, I do not understand.
Engineering Melanoma Brick by Brick
The development and progression of melanoma is an extraordinarily complex process. Decades of research have revealed dozens of molecular changes and interactions critical for the transition – from point mutations to epigenetic reprogramming to cell-cell interactions. However, no single one of these events provides us with the necessary knowledge to invariably prevent or predict the development of the disease or to abolish it once it has progressed.
The above quote by Richard Feynman applies equally well to cancer biology as it does to lecturing on theoretical physics or rebuilding a car engine. Our mission is to move toward a complete understanding of human melanoma by engineering its progression in vitro, piece by piece, inside and out, and use this knowledge to drive discoveries in prevention, diagnostics & treatment. We take a “bedside-to-bench-to-bedside” approach, learning from clinical observations then working to reconstruct both the observed three-dimensional microenvironment in which the cancer resides as well as the cancer’s genome.
We use then these models to:
- Ask, on a single cell level, what is the oncogenic penetrance of a particular mutation?
- Define the factors that drive or stabilize functional gene networks including:
o Transcription Factors
- Investigate the role of stochasticity in melanoma progression
The cells constituting benign nevi (left) and melanomas (right) are defined by both the external microenvironment and internal gene expression, such as the miRNA-regulated networks shown here.
We use a variety of tools, including genome editing, reconstituted skin culture, genetic interaction mapping and holographic imaging (shown here).
The Judson lab is currently funded by the Sander Fellows Program, the NIH DP5 Early Independence Award, the UCSF Department of Dermatology, the Helen Diller Family Comprehensive Cancer Center Impact Grant & the Sandler Program for Breakthrough Biomedical Research.