Philip J. Moos

The Moos laboratory is broadly interested in understanding cancer susceptibility and the development of resistance. Research efforts are focused on cancer genomics, mechanisms of disease, modifiers of cancer risk, and drug susceptibility.

Current work is primarily in three arenas: 1) tumor heterogeneity and the role genotype and phenotype in the response to therapeutics during cancer progression, 2) combining genomics and drug screens to identify novel therapeutic agents, and 3) genomic evaluation of nanoparticles for inflammatory potential or other toxic adverse effects.

The first and second area of research are collaborations with Dr. Bild and focus on tumor heterogeneity. Most tumors are thought to have monoclonal origin but by the time they are diagnosed, they are heterogeneous in terms of the subclonal structure driving their growth. We are involved in a collaboration where we are using various genomic strategies, from whole genome sequencing to single cell-RNA sequencing to elucidate the subclonal structure and pathways that dominate the subclones. We are also testing unique drugs and drug combinations to identify new potential strategies for therapeutic intervention.

The third and newer, area of research utilizes transcript profiling and apoptotic studies to evaluate particulate matter toxicity and inflammatory potential. We have found that certain metal oxide manufactured nanoparticles have significant toxicity and induce a cellular response to the stress of the nanoparticles. Nanomaterials provide many benefits and are being utilized more broadly so it is important to understand the potential toxicities, and mitigation strategies prior to use. Therefore, we collaborate with Dr. Ghandehari to understand the basis of the toxicology of materials with the potential for biomedical application. We also collaborate with Dr. Reilly to evaluate the genomic consequences of airborne pollutants that are risk factors for diseases like asthma