* denotes a publication that resulted from CTD2 intra-Network collaborations
CTD2 researchers showed that ovarian cancer patients with CD3+ tumor infiltrating lymphocytes and homologous recombination deficiency have improved survival.
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.
Researchers profiled 225 metabolites in 928 cell lines from more than 20 cancer types in the cancer cell line encyclopedia using liquid chromatography – mass spectrometry.
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.