Activating mutations in EGFR or RAS lead to aggressive cancers and are associated with poor patients’ prognoses. There is no therapy for some of the most aggressive EGFR/RAS cancers. Decades of intense research in diverse tumor models have highlighted the complexity of oncogenic Egfr/Ras signaling. Oncogenic Egfr/Ras operate via a broader than previously thought and more complex network of interacting signals.  While efforts to elucidate the nature and mechanisms of cell-intrinsic signaling interactions are providing significant insights, much less is known about Egfr/Ras-mediated  cell-cell interactions in the tumor milieu. Cell-cell interactions promote cancer progression and resistance to therapies. The underlying mechanisms remain elusive. Our laboratory uses integrated genetics, cell, and molecular biology approaches in complementary tumor models (Drosophila, human cancer cells, and mice) to identify novel and potentially clinically actionable cell-cell interaction mechanisms promoting tumor overgrowth and metastasis. One specific area of interest is the role of microvesicles in tumor progression, as well as tissue development.  Tumor cells pack bioactive cargo into plasma membrane-derived vesicles (microvesicles) to corrupt stromal cells and drive tumor overgrowth, metastasis, and drug resistance. We are investigating the basic molecular mechanisms controlling cargo sorting and microvesicle biogenesis, and are seeking an understanding of how microvesicle-mediated signals promote Egfr/Ras tumors. These efforts have the potential to expose molecular vulnerabilities that can be targeted to suppress and/or to re-sensitize Ras tumors to currently available therapies. Separate from these mechanistic studies, we are exploiting microvesicle biology for biomarkers applications.

We are recruiting highly motivated and result-driven graduate students to join our team. Please direct your inquiries to “”.