Henske Lab Discoveries
- Our laboratory was the first to discover the physical interaction between the TSC1 and TSC2 proteins (Cancer Research, 1998).
- Our lab first discovered that all three components of angiomyolipomas arise from a common precursor cell (American Journal of Pathology, 2003).
- We found a distinctive abnormality of amino acid sensing in Tsc1 and Tsc2-deficient S. Pombe (Journal of Biological Chemistry, 2004).
- We discovered that the Notch signaling pathway is active in angiomyolipoma-derived cells and that the Notch pathway is activated in Drosophila models of TSC (Journal of Clinical Investigation, 2010).
- Our lab discovered that autophagy and the autophagy substrate p62/Sequestosome1are critical to the in vivo growth of TSC2-null cells (PNAS, 2011).
- Our high-throughput drug screen identified chelerythrine as a selective death inducer in TSC2-deficient cells, demonstrating hypersensitivity to oxidative stress-depending cell death (Molecular Cancer Research, 2015).
- Through whole exome sequencing, we found that TSC2, and less commonly TSC1, alterations are the primary essential driver event in angiomyolipoma/LAM, and that somatic mutations rarely contribute to tumor development in this setting (PLoS Genetics, 2016).
- Our lab performed the first metabolomic profiling of ChRCC, revealing an unexpected defect in the gamma-glutamyl cycle, and glutathione salvage pathway, with key therapeutic implications (PNAS, 2018).
- We demonstrated the efficacy of checkpoint blockade in preclinical models of TSC and LAM (Journal of Clinical Investigation Insight, 2018).