* denotes a publication that resulted from CTD2 intra-Network collaborations
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.
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.
CTD2 scientists at OHSU demonstrated that sequential therapy with PARP and either WEE1 or ATR inhibitors is effective and potentially less toxic in multiple relevant cancer models.
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.