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
Johns Hopkins CTD2 scientists used population genetics in organoids model system to study heterogeneity and identify molecular mechanisms of metastasis in cancer.
Johns Hopkins University CTD2 scientists identified that Twist1 promotes metastasis by transcriptionally activating protein kinase D1 (Prkd1). Genetic and pharmacologic inhibition of Prkd1 indicated that Prkd1 drives tumor invasion, loss of cell-cell adhesion, and migration in basal breast cancer.
In vitro, in vivo, and patient cohort studies indicate that cannabinoids promote progression of HPV positive head and neck squamous cell carcinoma through p38 MAPK activation.
Scientists demonstrate that partial knockdown of MAP4K4 replaces SV 40 small T antigen component of STRIPAK. Study suggests that MAP4K4 is a key substrate for serine/threonine phosphatase, PP2A, and promotes oncogenic transformation through activation of the Hippo pathway effector, YAP1.
Computational analysis of two large-scale independent CRISPR-Cas9 viability screens performed at the Broad and Sanger Institutes indicate reproducible findings in identifying gene dependencies.
Researchers identify that mechanistic target of rapamycin (mTOR) kinase inhibitor, PP242 induces cell death in glioblastoma cells by off-target inhibition of both protein kinase C alpha and Janus kinase 2 (JAK2).
Scientists compared performance of RNA-Seq processing pipelines for the expression quantification of long non-coding RNAs (lncRNAs) in cancer samples. This study indicates integrating pseudoalignment methods with transcriptome annotation is a recommended strategy for RNA-Seq analysis of lncRNAs.
CTD2 scientists at DFCI performed genome-scale open reading frame screens to identify mechanisms of resistance to androgen deprivation therapy. This study shows that transcription factor, CREB5, is overexpressed and mediates resistance to androgen receptor antagonists in prostate cancer.
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