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 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.
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.
Researchers analyzed The Cancer Genome Atlas multidimensional “omic” data using the stems-biology approaches. This study identified that the Hippo signaling pathway plays a critical role in tumor progression in squamous cell carcinoma and could be a potential therapeutic target.
This manuscript presents the molecular characteristics and drug exposure response for a large number of clinically well annotated adult AML cases. These data will reveal potential novel treatment options that will be tested in clinical trials.
CTD2 scientists demonstrated that the myoepithelial cells block luminal epithelial cell dispersal. This depends on the smooth muscle contractility and adhesion.
CTD2 researchers at DFCI systematically analyzed loss-of-function screens in cancer cell lines combined with TP53 mutagenesis screens. These studies determined the function of every possible missense or nonsense TP53 mutations and have shown increased cell proliferation.
Integration of functional proteomics, systems biology, and molecular biology studies identified mTORC1 functions as a mediator between nutrition availability sensing and determinant for G2/M checkpoint recovery.
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