Publications
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
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.
Scientists studied the mechanisms of resistance to neoadjuvant therapy in triple-negative breast cancer and identified mitochondrial oxidative phosphorylation as a potential dependency, a nongenomic mechanism of resistance.
UCSF scientists developed a searchable database of the synthetic lethal screen https://mmues.shinyapps.io/K7screen/ generated by performing a saturation screen with an ultra-complex shRNA library containing 30 independent shRNAs per gene target in cell lines treated with PI3K inhibitor.
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.
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.
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