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

 

CTD²
November 14, 2014
PLoS One

Researchers suggest that glioblastoma (GBM) patients whose tumors carry mutant PIK3R1 alleles may benefit from treatment with inhibitors of AKT.

CTD²
October 26, 2014
Nature Genetics

Researchers identify somatic mutations in RNF43 in over 18% of colorectal adenocarcinomas and endometrial carcinomas, which encodes an E3 ubiquitin ligase that negatively regulates Wnt signaling.

CTD²
October 23, 2014
Cell Reports

These results suggest that benzodiazepines may have clinical potential for neuroblastoma therapy.

CTD²
October 23, 2014
Cell

The authors construct genome-scale CRISPRi and CRISPRa libraries. Growth-based screens identify essential genes, tumor suppressors, and regulators of differentiation.

CTD²
October 17, 2014
ACS Chemistry Biology

The small-molecule probes STF-31 and its analogue compound 146 were discovered while searching for compounds that kill VHL-deficient renal cell carcinoma cell lines selectively. Cell lines showed sensitivity to three different inhibitors of nicotinamide phosphoribosyltransferase (NAMPT).

CTD²
October 14, 2014
PLoS One

Researchers present CINDy (Conditional Inference of Network Dynamics), a novel algorithm for the genome-wide, context specific prediction of regulatory post-translational dependencies between signaling protein and transcription factor activity, from gene expression data.

CTD²
October 14, 2014
PNAS

By combining whole-genome microarray expression analysis on lung cancer cell lines with ChIP-Seq data, the authors discover an ASCL1 target 72-gene expression signature.

CTD²
October 10, 2014
The Journal of Investigative Dermatology

Researchers discuss insights of cancer biology learned from using skin carcinogenesis as a model. 

 

CTD²
October 09, 2014
Cell

We also use the SunTag to create a potent synthetic transcription factor by recruiting multiple copies of a transcriptional activation domain to a nuclease-deficient CRISPR/Cas9 protein and demonstrate strong activation of endogenous gene expression and re-engineered cell behavior.

CTD²
October 09, 2014
Cell

The authors propose a framework for the systematic discovery of genetic alterations that are causal determinants of disease.

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