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
Broad Institute CTD2 scientists identified cytochrome P450 oxidoreductase as an essential factor for ferroptotic cell death in cancer using genome-wide CRISPR-Cas9 suppressor screens.
CTD2 scientists at UCSF used CRISPR interference approach to study gene-specific expression–phenotype relationships and expression level-dependent cell responses at single-cell resolution. This technique could be used in drug development, functional genomics, and identification of suppressor.
Scientists performed WGS, RNA and T-cell receptor sequencing, immunohistochemistry and reverse phase protein array proﬁling on pediatric and adult samples. Study indicated that genomic complexity causes immunosuppressive phenotype and provides opportunities for developing novel treatments.
Risk stratification of medulloblastoma subtype could minimize the burden of cerebellar mutism syndrome burden on pediatric patients with posterior fossa tumors, a type of brain tumor located in or near the bottom of the skull.
Report on challenges and opportunities associated with translating basic science discoveries in glioblastoma discussed during the neuro-oncology community meeting in April 2019.
Stanford University used single-cell genomics to characterize heterogenous cell types and states in tumor microenvironment revealing changes in transcriptional states, regulatory networks, and intercellular communication between matched gastric tumor and normal tissue from same patients.
Human pluripotent stem cells-derived natural killer cells have improved antibody-dependent cellular cytotoxicity and could be used to treat refractory malignancies.
Scientists analyzed whole genomes of over 2500 tumors from 27 different cancer types and identify new components of cancer pathways that are altered by coding and non-coding mutations.
Phase II clinical trial with single-agent Akt inhibitor, MK2206, in recurrent platinum-resistant high-grade serous ovarian cancers with molecular aletarions in PI3K/AKT pathway is not effictive.