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
Cancer Cell Line Encyclopedia, provides a detailed genetic characterization of human cancer cell lines from gene to transcript to protein. Integration of this data with chemical and genetic perturbation data reveals potential therapeutic targets and biomarkers for cancer.
Perspective on the role of tumor immune compartment, microenvironment, heterogeneity, and epigenetics during cancer pathogenesis and development of treatment resistance.
Texomer, a statistical approach, improves molecular characterization of cancer samples by integrating cancer genome and transcriptome sequencing data obtained from patient tissue samples.
Genome-wide CRISPR-Cas9 screen identifies bromodomain-containing protein 9, a subunit of chromatin remodeling complex, SWI/SNF, as a therapeutic target in SMARCB1-deficient pediatric malignant rhabdoid tumors.
UCSF (2) CTD2 scientists discovered a key dendritic cell-type, cDC2, as being critical to prime CD4+ T cells for antitumor functions. They also identified a pathway, regulated by T-regulatory cells, that modulates the ability of these cells to drive protective immunity.
Study shows that pancreatic cancer patients with high levels of tumor suppressor, protein kinase C, and low levels of phosphatase, PHLPP1, have improved survival.
Scientists studied the mechanisms of resistance to neoadjuvant therapy in triple-negative breast cancer and identified mitochondrial oxidative phosphorylation as a potential dependency, a nongenomic mechanism of resistance.
UCSF scientists developed a searchable database of the synthetic lethal screen https://mmues.shinyapps.io/K7screen/ generated by performing a saturation screen with an ultra-complex shRNA library containing 30 independent shRNAs per gene target in cell lines treated with PI3K inhibitor.
CTD2 scientists at Broad Institute integrated genome-wide CRISPR screening and lipidomic profiling and identified the hypoxia-inducible factor pathways as an intrinsic vulnerability to ferroptosis. This vulnerability can be exploited by inhibiting glutathione peroxidase 4 in clear-cell carcinomas.