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
DFCI scientists identified XL177A as potent irreversible inhibitor of USP7, a deubiquitinating enzyme. This study indicated that TP53 mutational status predicted inhibitory response across several cancer lineages; demonstrates TP53 mutational status as a biomarker for response to USP7.
Chemical biology approach reveals metabolic heterogeneity in cellular subtypes. This study suggests targeting both glucose reporter 1 and pyruvate dehydrogenase, components of glycolysis and mitochondrial metabolism, inhibit cancer cell invasion.
Study showed that combinatorial therapy with MLN4924, a drug that clears misfolded proteins, and anti-PD1, an immune-checkpoint blockade, enhances clinical responses in cancer patients with microsatellite instability.
Scientists at Stanford CTD2 Center showed that MethylMix, a tool to identify methylation driver genes in cancer, can predict DNA methylation profiles in whole slide cancer histopathology images. This analysis provides new insights into the link between histopathological and molecular data.
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.
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.