* denotes a publication that resulted from CTD2 intra-Network collaborations
Chemical biology approach reveals metabolic heterogeneity in cellular subtypes. This study suggests targeting both glucose reporter 1 and pyruvate dehydrogenase, components of glycolysis and mitochondrial metabolism, inhibit cancer cell invasion.
In vitro and in vivo studies conducted by CTD2 scientists at Emory University demonstrate that combination of JNK inhibitor, AS602801 with androgen receptor inhibitor, enzalutamide synergistically inhibit proliferation, migration, invasion, and prevent tumor growth in prostate cancer.
Scientists at Stanford CTD2 Center showed that MethylMix, a tool to identify methylation driver genes in cancer, can predict DNA methylation profiles in whole slide cancer histopathology images. This analysis provides new insights into the link between histopathological and molecular data.
Researchers emphasize the influence of inherited germline variants in immune infiltration patterns of the tumor microenvironment. This study may help in understanding the predictors of response to immunotherapy.
Broad Institute CTD2 scientists identified cytochrome P450 oxidoreductase as an essential factor for ferroptotic cell death in cancer using genome-wide CRISPR-Cas9 suppressor screens.
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.