Publications
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
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.
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 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.
Columbia CTD2 researchers developed ADVOCATE, a computational model to analyze gene expression data of epithelial and stromal pancreatic ductal adenocarcinoma samples. These studies indicated a novel classification signature which could facilitate the development of precision oncology approaches.
Scientists at the UCSD CTD2 Center showed that epigenetic dysregulation and silencing are associated with chromatin repression and aberrant hypermethylation at the transcription start site in HPV-related oral cancers; independent of CpG island and is associated with MYC pathway activation.