* denotes a publication that resulted from CTD2 intra-Network collaborations
Publications
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.
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.
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.
Texomer, a statistical approach, improves molecular characterization of cancer samples by integrating cancer genome and transcriptome sequencing data obtained from patient tissue samples.
Perspective on the role of tumor immune compartment, microenvironment, heterogeneity, and epigenetics during cancer pathogenesis and development of treatment resistance.
Cancer Cell Line Encyclopedia, provides a detailed genetic characterization of human cancer cell lines from gene to transcript to protein. Integration of this data with chemical and genetic perturbation data reveals potential therapeutic targets and biomarkers for cancer.
Researchers profiled 225 metabolites in 928 cell lines from more than 20 cancer types in the cancer cell line encyclopedia using liquid chromatography – mass spectrometry.
Genome-wide CRISPR-Cas9 screen identifies bromodomain-containing protein 9, a subunit of chromatin remodeling complex, SWI/SNF, as a therapeutic target in SMARCB1-deficient pediatric malignant rhabdoid tumors.
Protein Kinase C Quality Control by Phosphatase PHLPP1 Unveils Loss-of-Function Mechanism in Cancer.
Study shows that pancreatic cancer patients with high levels of tumor suppressor, protein kinase C, and low levels of phosphatase, PHLPP1, have improved survival.
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