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
The authors analyzed cellular perturbation profiles to identify established MoA proteins for 70% of tested compounds.
Researchers find that RAS pathway activation can act as a biomarker for sensitivity of ovarian cancer cells to decitabine.
Researchers report mTORC1 activation suppresses proliferation when cells rely on extracellular proteins as an amino acid source, and these results may have important implications for the use of mTOR inhibitors as therapeutics.
The authors analyzed a discovery set of 13 CCSKs for changes in chromosome copy number, mutations, rearrangements, global gene expression and global DNA methylation.The study reported significant hypermethylation of TCF21 and/or decreased TARID expression in the cases of most CCSKs.
Researchers optimize several aspects of shRNA libraries to create next-generation high-complexity mouse and human shRNA libraries.
Researcehrs show human colorectal cancers (CRC)cells can revert to functioning normal cells given appropriate signals and provide compelling in vivo validation of the Wnt pathway as a therapeutic target for treatment of CRC.
Researchers introduce a cell culture medium that enables routine establishment of cell lines from human ovarian cancers which retain the genomic landscape, histopathology and molecular features of the original tumours.
Researchers introduce a sequential trimming-and-retrieving alignment approach for investigating DNA methylation patterns, which significantly improves the number of mapped reads and covered CpG sites.
Researchers performed genomewide analyses of 293 lower-grade gliomas from adults, incorporating exome sequence, DNA copy number, DNA methylation, messenger RNA expression, microRNA expression, targeted protein expression, and tested for correlation with clinical outcomes.
Investigators determine the molecular mechanism of the chemotherapeutic agent didemnin B and find a biomarker to predict sensitivity.