* denotes a publication that resulted from CTD2 intra-Network collaborations
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.
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.
CTD2 scientists demonstrated that the myoepithelial cells block luminal epithelial cell dispersal. This depends on the smooth muscle contractility and adhesion.