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
CTD2 scientists at Stanford University demonstrated that air-liquid interface patient-derived tumor organoid models retain the original tumor immune cells, enabling testing for personalized immunotherapy in cancer.
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.
CTD2 researchers at Emory University identify novel role for large tumor suppressor 2, LATS2, as a regulator of the ASK1-mediated stress response pathway which may lead to new strategies to control cellular response to stress in normal cells and diseases.
UCSF scientists developed a bioinformatic approach, MAGNETIC, which integrates multi-omic data from cancer patients with pharmacogenomic data from cell lines into a small set of pathway-enriched gene modules. These modules connect tumor and cell line biomarkers and may inform therapeutic targets.
UCSF (1) CTD2 researchers identified a synthetic lethal interaction between EGFR tyrosine kinase inhibitors and Aurora kinase inhibitors in acquired resistant cells. This study suggests combinatorial treatment to prevent treatment resistance with the monotherapies.
CTD2 scientists at Oregon Health and Science University performed genetic and small-molecule screens and identified CSF1R as a novel therapeutic target of acute myeloid leukemia.
Study demonstrates that EGFR and EGFRvIII cooperate through KRAS, to upregulate chemokine CCL2 and promote infiltration of macrophages in glioblastoma.
CTD2 scientists studied the functional consequences of missense mutations of cell surface protein kinase receptor, PDGFRA, identified from different tumor types. These studies identified a driver mutation in the extracellular domain of PDFRA that are resistant to PDFR inhibitors.
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