Publications
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
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.
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.
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.
Bioinformatics analysis of The Cancer Genome Atlas (TCGA) data identifies focal adhesion kinase as a potential therapeutic target for uveal melanoma.
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.
Human primary liver cancer organoids reveal intratumor and interpatient drug response heterogeneity.
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.
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.
Computational analysis of laser capture microdissection and RNA sequencing data established a novel classification signature of molecular subtypes in pancreatic ductal adenocarcinoma.
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