477 Publications Available
April 08, 2019
Nature Communications

CTD2 scientists at Broad Institute integrated genome-wide CRISPR screening and lipidomic profiling and identified the hypoxia-inducible factor pathways as an intrinsic vulnerability to ferroptosis. This vulnerability can be exploited by inhibiting glutathione peroxidase 4 in clear-cell carcinomas.

March 22, 2019

Review on the mechanisms of regulating oncogenic RAS signaling pathway in cancer and strategies for drugging “undruggable” targets.

March 21, 2019
Cancer Research

Dana-Farber Cancer Institute scientists analyzed data from genome-wide RNAi and CRISPR-Cas9 screens. Results of this study showed the hypoxia-inducing factor, EGLN1, as a preferential and druggable cancer dependency in a subset of cancer cell lines.

March 18, 2019
Molecular Cell

Study shows that pancreatic cancer patients with high levels of tumor suppressor, protein kinase C, and low levels of phosphatase, PHLPP1, have improved survival.

March 15, 2019
Cancer Discovery

Patient-derived in vitro and in vivo model systems discovered novel gene fusion, LAMTOR1-AKT1, as a tumorigenic driver in pediatric epithelioid neoplasm.

March 12, 2019

Integration of genetic and chemical screens identified a synthetic lethal relationship between SMARCB1-deficient cancers and the ubiquitin-proteasome system.

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.

March 04, 2019
Current Opinion in Genetics & Development
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.

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.