* denotes a publication that resulted from CTD2 intra-Network collaborations
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 researchers at the University of California, San Francisco showed that ROS1 fusion oncoproteins exhibit differential activation of MAPK signaling pathway in lung adenocarcinoma.
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.
Scientists at JHU showed that there is an intra-tumor and inter-patient heterogeneity to drug responses in patient-derived primary liver organoids. These studies indicate the potential use of pre-clinical organoid models in screening small-molecules and identifying novel targets.
OHSU CTD2 scientists identify distinct patterns of mutation dynamics during FLT3 inhibitor, crenolanib treatment in acute myeloid leukemia. This study indicates comprehensive sequencing should be carried before and during the treatment to identify combinatorial agents and prevent drug resistance.
Study identifies networks of DNA damage-up proteins that may predict tumorigenic functions of cancer-promoting proteins.
CTD2 researchers developed phospho-proteomic specific algorithm, pARACNe, which measures phospho-state dependencies between tyrosine kinases and their candidate substrates from large-scale LC-MS/MS phosphoproteomic profiles.