During cancer development, cells evade important regulatory controls, resulting in increased cell proliferation and cell survival, and, for solid tumors, loss of cell polarity and an increased ability to migrate and invade tissues. My lab aims to dissect these major cellular controls that are utilized during normal development and that are perturbed during tumorigenesis.

I have developed simple Drosophila models that address isolated aspects of cancer development, exploiting the conservation of Drosophila and vertebrate biology. Advantages of Drosophila include its genetic versatility and low genetic redundancy, as well as the powerful technology of genome-wide RNA interference (RNAi) by double stranded RNA (dsRNA) in Drosophila tissue culture. My lab currently focuses on two major lines of research:

(1) Cell survival and development in the Drosophila hematopoietic system.

I have demonstrated a role for PDGF/VEGF receptors in cell survival, a function that is paralleled between Drosophila and human hematopoiesis and that is aberrant in a number of leukemias and other malignancies. Subsequently, I utilized this system to conduct a cell-based genome-wide RNAi screen to identify novel genes that modify this pathway.

(2) Epithelial plasticity in novel Drosophila tissue culture systems

More recently, I have developed novel Drosophila cell lines that for the first time allow the in vitro study of Drosophila epithelial plasticity related to tumor metastasis. Combined with RNAi screening, I identified potential modifiers of Dpp (a Drosophila TGFb-type ligand)- induced epithelial plasticity.

Employing both functional genomics and traditional single gene analysis, my lab further characterizes these genes of interest and validates their role across species. Our long-term goal is the identification of new gene functions and biological processes that play a role during normal development and tumorigenesis.