Immunology & Hematopoiesis
Green Lab
Abby Green, MD
Cancer develops through accumulation of DNA mutations and structural aberrations collectively known as genome instability. Genome damage in adult-onset malignancies can be traced to exogenous carcinogens or simply the process of aging. However, pediatric cancers do not arise as a result of aging or exogenous genotoxic agents. We are interested in the etiology of genome instability in pediatric cancers and the resulting genome-protective responses — also called DNA damage responses — that are activated. Our long-term goal is to identify predictors of mutagenesis and therapeutic vulnerabilities within DNA damage response pathways in order to develop new treatment options for children with cancer.
Morley Lab
S. Celeste Morley, MD, PhD
Up, down and all around. Immune cells are constantly in motion as they seek to defend the host against pathogens. Dramatic cell shape changes induced by alterations in the underlying actin cytoskeleton provide the structural framework required for cell motility.
Orvedahl Lab
Anthony Orvedahl, MD, PhD
We utilize a combination of hypothesis-driven and discovery-based approaches to understand factors that regulate host immune responses to infectious and sterile triggers of severe inflammation. We focus on the cytoplasmic recycling pathway of autophagy, which we found protected macrophages against cytokine-induced cell death and mice against fatal cytokine storm syndrome. However, the relative protective or pathogenic role of autophagy in macrophage survival remains unclear in different contexts. Preliminary findings point towards a critical intersection of these processes with immunometabolism. We are leveraging this experience and developing novel tools to understand the commonalities and peculiarities of cytokine storm syndromes triggered by various etiologies including SARS-CoV-2. The ultimate goal is to develop host-directed therapies for infectious and inflammatory disorders.