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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
Elife

Researchers discucss asparagine reliance of sarcoma cells may represent a metabolic vulnerability with potential anti-sarcoma therapeutic value.

CTD²
Nature Genetics

Researchers show that the androgen receptor cistrome undergoes extensive reprogramming during prostate epithelial transformation in man and establish the centrality of epigenetic reprogramming in human prostate tumorigenesis.

CTD²
Nature Communications

Investigators used ultra-pH-sensitive nanoparticles to study endosomes and lysosomes.

CTD²
Cold Spring Harbor Protocols

The combination of chemical carcinogens with genetically engineered mouse models has emerged as an invaluable approach to study the complex interaction between genotype and environment that contributes to cancer development.

CTD²
Cell Reports

The authors used network-based analysis of treatment signatures from GEM models to identify treatment-responsive genes in human prostate cancer that are potential biomarkers of patient response.

CTD²
Journal of Translational Medicine

Researchers identify Hepatocyte growth factor dependent signature may serve as a candidate predictive signature for patient enrollment in clinical trials using MET inhibitors.

CTD²
Oncotarget

Researchers find that activation of EGFR signaling leads to resistance of BRAF inhibitors, and that adding EGFR inhibitors increases the efficacy of BRAF inhibitor treatment.

CTD²
eLife

Researchers used a next-generation shRNA platform to screen for genes conferring resistance to carfilzomib in multiple myeloma cells.

CTD²
PNAS

Researcehrs describe the discovery of the small-molecule probe BRD5631, and demonstrate that BRD5631 affects several cellular disease phenotypes previously linked to autophagy.

TARGET
Nature Genetics

Whole-genome sequencing showed high frequency of mutations that were predicted to activate the RAS-MAPK pathway in relapse neuroblastoma samples as well as in neuroblastoma cell lines.