Stanford University used single-cell genomics to characterize heterogenous cell types and states in tumor microenvironment revealing changes in transcriptional states, regulatory networks, and intercellular communication between matched gastric tumor and normal tissue from same patients.
Study showed that combinatorial therapy with MLN4924, a drug that clears misfolded proteins, and anti-PD1, an immune-checkpoint blockade, enhances clinical responses in cancer patients with microsatellite instability.
Report on challenges and opportunities associated with translating basic science discoveries in glioblastoma discussed during the neuro-oncology community meeting in April 2019.
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.