* denotes a publication that resulted from CTD2 intra-Network collaborations
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.
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.
CTD2 researchers showed that ovarian cancer patients with CD3+ tumor infiltrating lymphocytes and homologous recombination deficiency have improved survival.
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.
Study shows that pancreatic cancer patients with high levels of tumor suppressor, protein kinase C, and low levels of phosphatase, PHLPP1, have improved survival.