The Moos laboratory is broadly interested in understanding inflammation and cancer susceptibility. Research efforts are focused on transcriptomics, mechanisms of disease, modifiers of risk, and drug susceptibility.
Current work is primarily in three arenas: 1) the role of phenotype in the response to therapeutics during cancer progression, and combining genomics and drug screens to identify novel therapeutic agents, 2) identifying mechanisms of psychiatric conditions using single-cell and spatial transcriptomics, and 3) transcriptomic evaluation of inflammatory conditions and other toxicants as early factors in disease. The Moos lab applies techniques like single-cell transcriptomics and drug screens to these areas of interest.
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. The Moos lab is involved in a collaborations where we are using various genomic strategies, from whole genome sequencing to single cell-RNA sequencing and drug screens to elucidate the tumor susceptible pathways that dominate the subclones. We are also testing unique drugs and drug combinations to identify new potential strategies for therapeutic intervention.
The Moos lab is new to neurosciences but we have built collaborations to utlize single-cell and spatial transcriptomics to generate insight into neurological conditions primarily through animal model systems but we intend to also evaluate these conditions in human samples.
Inflammation can be a risk factor for cancer development as well as other disease states. The third area of research utilizes transcript profiling to determine what cells are involved in inflammatory conditions and to elucidate how they may communicate. The intention is to identify therapeutic targets that we can modulate. We collaborate with Drs. Reilly and Venosa utilizing animal models and human cells to evaluate the genomic consequences of air.