CTD2 scientists at Broad Institute integrated genome-wide CRISPR screening and lipidomic profiling and identified the hypoxia-inducible factor pathways as an intrinsic vulnerability to ferroptosis. This vulnerability can be exploited by inhibiting glutathione peroxidase 4 in clear-cell carcinomas.
Perspective on the role of immune system in different tissues and how it contributes to disease when the prototype gets dysregulated or dysfunctional.
Review on the mechanisms of regulating oncogenic RAS signaling pathway in cancer and strategies for drugging “undruggable” targets.
Scientists at the Emory University CTD2 Center developed the High-Throughput immunomodulator Phenotypic (HTiP) screening platform to explore PPI inhibitors, as immunomodulators. This screening identified the Inhibitor of Apoptosis Protein (IAP) as anti-tumor immunity enhancers.
Dana-Farber Cancer Institute scientists analyzed data from genome-wide RNAi and CRISPR-Cas9 screens. Results of this study showed the hypoxia-inducing factor, EGLN1, as a preferential and druggable cancer dependency in a subset of cancer cell lines.
Bioinformatics analysis of The Cancer Genome Atlas (TCGA) data identifies focal adhesion kinase as a potential therapeutic target for uveal melanoma.
Patient-derived in vitro and in vivo model systems discovered novel gene fusion, LAMTOR1-AKT1, as a tumorigenic driver in pediatric epithelioid neoplasm.
Integration of genetic and chemical screens identified a synthetic lethal relationship between SMARCB1-deficient cancers and the ubiquitin-proteasome system.
Concurrent measurement of single cell expression in tumor cells and tumor-infiltrating lymphocytes revealed novel biological insights of the tumor microenvironment; provides basis for developing novel therapeutic targets in lymphoma.