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 scientists at UCSF (1), Broad Institute, and TGen have identified that drug-tolerant persister cancer cells from multiple tumor types that survive chemotherapy were found to be vulnerable to chemical inhibition or genetic loss of function of GPX4.
TARGET’s AML researchers identified abundant expression of miR-106a, a marker for treatment resistance, in relapsed and refractory pediatric AML through a comprehensive miRNA profile to identify potential biomarkers as predictors for improved outcomes.
Scientists found that overexpression of PRAS40 in lung adenocarcinoma and cutaneous melanoma was associated with poor prognosis. This study describes a novel protein interaction signaling node where PRAS40 can increase NF-κB transcriptional activity through physical association with P65.
Scientists use hydrocarbon peptide stapling to develop cell permeable and stabile peptides capable of blocking RAB25-FIP complex formation. These peptides inhibit RAB25-depenent (pro- and anti-tumorigenic) phenotypes in cancer cells.
The CTD2 Dashboard is an interactive web interface which compiles conclusions with associated supporting evidence. This open access resource makes the data findable, accessible, interoperable and reusable to both computational and non-computational experts.
CTD2 scientists developed an Onco-GPS tool—a data-driven approach useful in establishing relationships—to explore cancers with altered RAS/MAPK. These components help to map individual samples onto a novel visual paradigm and strategize therapy against cancers with well-defined oncogenic lesions.
TARGET researchers performed comprehensive analysis of Wilms Tumors and identified convergence of numerous genetic changes on limited developmental pathways resulting in oncogenesis. Findings suggests targeting common pathways is better for intervention instead of individual gene mutations.