Our research is dedicated to deconstructing the multistep process of tumorigenesis. The major emphasis of our laboratory is to uncover the pathways that are disabled by mutational inactivation of tumor-suppressor genes as well as those pathways stimulated by aberrant oncogene activation. Areas of interest within the laboratory include: p53-regulated tumor immune surveillance, Rb-mediated tumor suppression, chemical genetic strategies to modulate tumor suppression, development of gene regulating tools for mouse models, and Kras signaling in lung cancer.

The Feldser lab uses genetically engineered mouse models to study tumor progression and metastasis of common forms of human cancer. These models faithfully recapitulate many aspects of the histopathological progression of their human counterparts. Tumors initiate within the appropriate tissue microenvironment from single cells due to induced activation of latent oncogenes and/or deletion of key tumor suppressor genes. These lesions evolve through multiple cellular states toward malignant and metastatic disease. We focus on mouse models in order to employ novel genetic tools to regulate gene function at will in developing cancerous lesions as well as track cancer growth and dissemination via bioluminescent and fluorescent techniques. We couple cellular, genomic and biochemical analyses to our powerful in vivo tools to discern the mechanics of tumor progression and metastasis with the goal of identifying new therapeutic strategies to eradicate malignant cells.