How do cells with the same genetic material build systems that vary in form and function? This question lies at the heart of developmental biology in mammals. Our hypothesis is that mammalian cells contain gene programs that naturally give rise to variation within cell populations. These gene network structures may be exploited by cancers, driving tumor heterogeneity and treatment failure. We test these ideas with a combination of cell biology, genomics, bioinformatics, and technology development.
Many genes show highly heterogeneous expression across populations of cells, with high expression in some cells and low expression in other cells
Ultimately, cells must organize genes into functional modules of coexpression. How does this process occur and how does it break down in cancer?
A part of what may drive tumors is the activation of developmental programs in the wrong time and place. But which programs in which tumors? We're building maps of each tumor's developmental characteristics and using them to build novel cancer diagnostics using deep learning artificial intelligence approaches.
