* denotes a publication that resulted from CTD2 intra-Network collaborations
Publications
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.
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.
Protein Kinase C Quality Control by Phosphatase PHLPP1 Unveils Loss-of-Function Mechanism in Cancer.
Study shows that pancreatic cancer patients with high levels of tumor suppressor, protein kinase C, and low levels of phosphatase, PHLPP1, have improved survival.
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.
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.
Researchers developed PTMsigDB, a database of post-translational modifications, such as site-specific phosphorylation signatures of kinases, perturbations, and signaling pathways, curated from more than 2,500 publications.
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.
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