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
CTD2 researchers report improved interpretability of the EDDY-CTRP results by using STITCH (protein) and STRING (drug)-interaction databases to generate evidence networks of drug-mediator pairs. These evidence networks will provide insights to drug sensitivity.
CTD2 investigators at DFCI identified genes required for the survival of cancer cells in the presence of PI3K inhibition using genome-scale shRNA-based apoptosis screens.
Review on the emerging paradigm of reactive oxygen species function as specific, intracellular secondary messengers rather than as binary, indiscriminate, damaging molecules in cancer.
CTD2 researchers at Dana Farber Cancer Institute identify genome editing by CRISPR-Cas9 and gene suppression by CRISPRi have different off-target effects and combining these approaches provides complementary information in loss-of-function genetic screens.
Researchers characterized the role of the transcription repressor ZBTB18 as a putative tumor suppressor in mesenchymal subtype of glioblastoma.
CTD2 investigators developed a novel technology which permits fusion gene construction for functional evaluation. Using this methodology, they validated five novel fusion genes as potential drivers for cancer.
CTD2 scientists surveyed alterations in PI3K/Akt/mTOR pathway across 10,000 human cancers profiled by TCGA. This study generated a comprehensive and annotated catalog of variants which may serve as a precision medicine approach to stratify patients by mutation type.
CTD2 researchers at Dana Farber identify that 2-oxoglutarate dehydrogenase, a tricarboxylic acid cycle enzyme, is crucial to maintain PIK3CA mutant tumor survival or proliferation.
Scientists demonstrate that Phosphoinositide 3-kinase enhancer (PIKE)-A directly interacts with CDK4. Furthermore, in vitro and in vivo studies in Glioblastoma (GBM) have shown that PIKE-A/CDK4 complex promotes cell proliferation and tumorigenesis.
CTD2 investigators at UCSF developed an orthogonal CRISPR/Cas-approach to quantify loss- and gain-of-function phenotypes. This approach can be used to systematically identify genetic interactions between cancer relevant genes that can in turn illuminate the genome.