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
March 04, 2019
Journal for ImmunoTherapy of Cancer

CTD2 scientists at the University of California, San Francisco showed that α-PD-1/α-TGFβ combinatorial therapy could be a potential treatment option for squamous cell carcinomas with high mutational load and form the basis for the clinical trial NCT02947165.

CTD²
March 01, 2019
Trends in Cancer

Review article discusses the mechanisms of resistance developed to cancer therapy and advantages of using intermittent therapies to maintain a balance between therapy-sensitive and therapy-resistant populations.

CTD²
March 01, 2019
Molecular & Cellular Proteomics

Researchers developed PTMsigDB, a database of post-translational modifications, such as site-specific phosphorylation signatures of kinases, perturbations, and signaling pathways, curated from more than 2,500 publications.

CTD²
March 01, 2019
Experimental Hematology

Review on using human pluripotent stem cells derived natural killer cells and macrophages as a novel cell-based approach for cancer immunotherapy.

CTD²
February 18, 2019
Molecular Cancer Research

Scientists at DFCI identified that genes MCL1 and DEDD contribute to aggressive urothelial carcinoma.

CTD²
February 13, 2019
Cell Metabolism

Systematic analyses of genetic and pharmacologic screening revealed that inhibition of deubiquitinases and glutathione synthesis blocks tumor growth.

CTD²
February 12, 2019
Cancer Research

DFCI scientists integrated data from large-scale RNAi, CRSIPR-Cas9, and small-molecule screens of malignant rhabdoid tumor cell lines and identified MDM2 and MDM4 as actionable targets.

CTD²
February 12, 2019
Nature Communications

Scientists show that loss of PIK3R1 in ovarian cancers activates AKT and JAK2/STAT3 signaling. These studies provide a rationale for mechanism-based combinatorial therapy with AKT and STAT3 inhibitors.

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