* denotes a publication that resulted from CTD2 intra-Network collaborations
Review on using human pluripotent stem cells derived natural killer cells and macrophages as a novel cell-based approach for cancer immunotherapy.
Review article discusses the mechanisms of resistance developed to cancer therapy and advantages of using intermittent therapies to maintain a balance between therapy-sensitive and therapy-resistant populations.
Researchers developed PTMsigDB, a database of post-translational modifications, such as site-specific phosphorylation signatures of kinases, perturbations, and signaling pathways, curated from more than 2,500 publications.
Scientists at DFCI identified that genes MCL1 and DEDD contribute to aggressive urothelial carcinoma.
Systematic analyses of genetic and pharmacologic screening revealed that inhibition of deubiquitinases and glutathione synthesis blocks tumor growth.
Scientists show that loss of PIK3R1 in ovarian cancers activates AKT and JAK2/STAT3 signaling. These studies provide a rationale for mechanism-based combinatorial therapy with AKT and STAT3 inhibitors.
DFCI scientists integrated data from large-scale RNAi, CRSIPR-Cas9, and small-molecule screens of malignant rhabdoid tumor cell lines and identified MDM2 and MDM4 as actionable targets.
CTD2 scientists identified the developmental transcription factor T as an essential gene in chordoma through genome-scale CRISPR-Cas9 screening. Small-molecule sensitivity profiling showed that CDK7/12/13 and CDK9 inhibitors inhibit chordoma cell proliferation.
CTD2 researchers at the University of California, San Francisco showed that ROS1 fusion oncoproteins exhibit differential activation of MAPK signaling pathway in lung adenocarcinoma.