Publications

UCSF CTD2 scientists developed a multi-faceted testing framework and demonstrate that analysis of protein networks rather than a single gene identifies synthetic lethal candidates. These candidates are reproducible as they are dependent on genetic and cellular context.

p85β regulatory subunit of phosphatidylinositol 3-kinase upregulates tyrosine kinase, AXL, activating p110 subunit to induce PDK1/SGK3 signaling in PIK3R2-amplified ovarian cancer. These findings indicate that targeting AXL with small molecule inhibitors could be a potential therapeutic strategy.

Scientists discovered point mutations in the ErbB2 receptor in a small subset of hematologic malignancies. These point mutations are shown to be oncogenic in cytokine-independent cellular assay and sensitive to irreversible ErbB inhibitors.

TransPRECISE, a cancer-specific integrated network estimation model, assesses pathway similarities between patients and cell lines at a sample-specific level. This framework bridges the gap and could be used to identify appropriate preclinical models for prioritizing specific drug targets.

Integrated analyses of multi-omics data indicate molecular and cellular differences in the clinical subtypes of high-grade serous ovarian cancer.

In vitro and in vivo studies conducted by CTD2 scientists at Emory University demonstrate that combination of JNK inhibitor, AS602801 with androgen receptor inhibitor, enzalutamide synergistically inhibit proliferation, migration, invasion, and prevent tumor growth in prostate cancer.

Protein dependency analytic module integrated in TCPA measures key cancer dependencies in a context dependent manner. This analysis suggests that protein expression data are a highly valuable information resource for understanding tumor vulnerabilities and identifying therapeutic opportunities.

DFCI scientists identified XL177A as potent irreversible inhibitor of USP7, a deubiquitinating enzyme. This study indicated that TP53 mutational status predicted inhibitory response across several cancer lineages; demonstrates TP53 mutational status as a biomarker for response to USP7.