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
Scientists analyzed whole genomes of over 2500 tumors from 27 different cancer types and identify new components of cancer pathways that are altered by coding and non-coding mutations.
Phase II clinical trial with single-agent Akt inhibitor, MK2206, in recurrent platinum-resistant high-grade serous ovarian cancers with molecular aletarions in PI3K/AKT pathway is not effictive.
CTD2 scientists developed a high-throughput in vivo complementation screening platform that enabled discovery of driver mutations of PIK3CA in glioblastoma. These studies highlight that variant function is context specific.
Studies indicate that Syk kinase plays a role in the control of macrophage-mediated immune suppression and inhibition of anti-tumor immunity. SRX3207, a dual inhibitor of PI3K and Syk kinases, inhibits macrophages polarization and activates innate and adaptive antitumor immunity in vivo.
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).
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