* denotes a publication that resulted from CTD2 intra-Network collaborations
Publications
Integrated analyses of multi-omics data indicate molecular and cellular differences in the clinical subtypes of high-grade serous ovarian cancer.
Integrated analysis of RNA-sequencing, proteomics, and phosphoproteomics data indicate doublecortin like kinase 1 (DCLK1) modulates proteins and pathways associated with cell motility in patient-derived pancreatic ductal adenocarcinoma (PDAC) organoids.
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.
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.
In vitro and in vivo studies conducted by CTD2 scientists at Emory University demonstrate that combination of JNK inhibitor, AS602801 with androgen receptor inhibitor, enzalutamide synergistically inhibit proliferation, migration, invasion, and prevent tumor growth in prostate cancer.
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.
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.
Conversations on mutism: risk stratification for cerebellar mutism based on medulloblastoma subtype.
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.
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