* denotes a publication that resulted from CTD2 intra-Network collaborations
Researchers emphasize the influence of inherited germline variants in immune infiltration patterns of the tumor microenvironment. This study may help in understanding the predictors of response to immunotherapy.
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.
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.
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.