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
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.
The study investigated the differences in chimeric read artifacts associated with formalin-fixed paraffin-embedded (FFPE) samples in molecular characterization studies by using a cohort of matched fresh-frozen (FF) and FFPE tissue samples.
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.
Scientists from BLGSP demonstrated that tumor EBV status defines a specific BL phenotype irrespective of geographic origin with particular molecular properties and distinct pathogenic mechanisms. EBV-positive BL genomes feature fewer driver mutations despite their greater mutational load.
UCSF (1) CTD2 researchers identified a synthetic lethal interaction between EGFR tyrosine kinase inhibitors and Aurora kinase inhibitors in acquired resistant cells. This study suggests combinatorial treatment to prevent treatment resistance with the monotherapies.