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 the UCSD CTD2 Center showed that epigenetic dysregulation and silencing are associated with chromatin repression and aberrant hypermethylation at the transcription start site in HPV-related oral cancers; independent of CpG island and is associated with MYC pathway activation.
CTD2 researchers showed that ovarian cancer patients with CD3+ tumor infiltrating lymphocytes and homologous recombination deficiency have improved survival.
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.
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.