The CTD² Network and Cancer Systems Biology Consortium organized a virtual symposium series titled “Multidisciplinary Approaches to Understand Cancer Treatment Resistance”. Please join us on 11/16, 11/17, 12/2, 12/16, and 12/17. Click here to view the registration website.
Publications
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.
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.
Protein Kinase C Quality Control by Phosphatase PHLPP1 Unveils Loss-of-Function Mechanism in Cancer.
Study shows that pancreatic cancer patients with high levels of tumor suppressor, protein kinase C, and low levels of phosphatase, PHLPP1, have improved survival.
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.
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.
Perspective on the role of immune system in different tissues and how it contributes to disease when the prototype gets dysregulated or dysfunctional.