Our research program investigates the role of cell surface tyrosine kinase receptors as cancer biomarkers and therapeutic targets. There are two areas of interest. The first area is the investigation into the mechanisms by which tyrosine kinase receptors affect tumor growth, malignant transformation and cancer cells response to chemotherapy. The second area focuses on translating the findings of these mechanistic studies to personalized target therapy for patients with cancers. Our long term goal is to provide a platform for rapid translation of basic science discoveries to innovative cancer clinical trials.
There are two projects in our laboratory. First, we are working towards understanding the mechanisms by which the Ron tyrosine kinase receptor confers malignant potential to head and neck cancer cells. Ron belongs to a family of multifunctional tyrosine kinase receptors which includes c-Met. Met is a well known oncogene. There are increasing evidences to suggest that Ron also behaves as an oncogene when overexpressed or became hyperactive. Ron overexpression has been consistently shown to play a role in the pathogenesis of several epithelial cancers. Preliminary studies in our laboratory suggest that Ron synergizes with EGFR, another well studied oncogene, in conferring aggressiveness in head and neck cancers. Therefore, we want to understand in greater depth the interplay between these two tyrosine kinase receptors. In return, we hope that this study will provide the basis for developing anti-Ron therapy to complement EGFR inhibitors in the treatment of head and neck cancers. Our second project involves understanding the role of EGFR mutations in a childhood cancer called neuroblastoma. We recently found that 20 – 30% of primary neuroblastic tumors express a novel EGFR extracellular deletion mutant that closely resemble the oncogenic variant EGFRvIII. We are working to define the oncogenic potential of this novel EGFR mutant in neuroblastoma. In addition, we are testing to see if the expression of this EGFR mutation affects neuroblastoma response to EGFR inhibitors. We hope that this study will yield information to support a personalized anti-EGFR treatment approach for neuroblastoma patients.