Included here is a list of publications from OCG programs. All published data are available to the research community through the program-specific data matrices.
* denotes publications from the CTD2 initiative that are results of intra-Network collaborations
Review on the mechanisms of regulating oncogenic RAS signaling pathway in cancer and strategies for drugging “undruggable” targets.
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.
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.
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.
CTD2 scientists at the University of California, San Francisco showed that α-PD-1/α-TGFβ combinatorial therapy could be a potential treatment option for squamous cell carcinomas with high mutational load and form the basis for the clinical trial NCT02947165.
Review article discusses the mechanisms of resistance developed to cancer therapy and advantages of using intermittent therapies to maintain a balance between therapy-sensitive and therapy-resistant populations.