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
Study reports that the third-generation pan-FGFR inhibitor, TAS-120, overcomes resistance to several FGFR2 mutations; leads to personalized targeted therapy in FGFR-activated intrahepatic cholangiocarcinoma.
Bioinformatic approach, MethylMix analysis, refines nominations for epigenetic driver genes by leveraging quantitative high-throughput proteomic data to select only genes where DNA methylation is predictive of protein abundance.
UCSF scientists demonstrated that neomorphic fusion oncoprotein, CIC-DUX4, controls capicua-regulated transcriptional pathways to promote hallmark features of malignancy like tumor cell survival, growth, and metastasis.
Study identifies acetylation as a regulatory mechanism leading ribonucleotide reductase activity, an enzyme that catalyzes the de novo synthesis of precursors required for DNA synthesis.
Review on the role of G protein-coupled receptors as part of cancer signaling networks promoting tumor growth, dissemination, and immune evasion in precision oncology and development of cancer immunotherapies.
Review on astrocyte diversity in the vertebrate central nervous system and their brain area and disease-specific properties and functions.
CTD2 scientists at Stanford University showed that radiomic analysis of computed tomography could be used to identify molecular subtypes of head and neck squamous cell carcinomas.
CTD2 scientists at Stanford University developed SCIMET, an analytical framework that provides quantitative measurement of dynamics of metastasis in a patient-specific manner; indicates early dissemination of colorectal cancer in the majority of the patients.
CTD2 scientists at OHSU demonstrated that sequential therapy with PARP and either WEE1 or ATR inhibitors is effective and potentially less toxic in multiple relevant cancer models.
Integrative genomic analyses of expression profiling, CRISPR-Cas9 and ORF/cDNA, identifies cell-essential genes suppressed by BET-bromodomain inhibition. The study suggests the use of cell-cycle inhibitors in combination with BET-bromodomain inhibitors to treat MYC-amplified medulloblastoma.