* denotes a publication that resulted from CTD2 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.
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.
CTD2 researchers at UCSF-1 present a quantitative map linking the influence of chemotherapeutic agents to tumor genetics. This chemical-genetic interaction map can aid in identifying new factors that dictate responses to chemotherapy and prioritize drug combinations.
Scientists have developed a cancer dependency map by combining off-target effects of RNAi and genomic characterization information across 501 cancer cell lines. The map facilitates identification and prioritization of therapeutic targets by predicting the genes essential for cell viability.