* denotes a publication that resulted from CTD2 intra-Network collaborations
Publications
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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.
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.
Plasticity of the cell state is proposed to drive resistance to multiple classes of cancer therapies. CTD2 researchers characterized this therapy-resistant cell state in human cancer cells and identify vulnerability to ferroptosis by inhibition of a lipid peroxidase.
CTD2 researchers at UTSW investigate alterations in oncogene-specific cellular signaling pathways in non-small cell lung cancer. BLC6 was identified as a target for combination therapy and may be potent way to overcome intratumor heterogeneity.
The authors use a loss-of-function screens and identified Prmt1, arginine methyltransferase as an essential oncogene and a regulator of translation. Therapeutic agents targeting Prmt1 and translation-associated pathways are potential treatment options for cancer.
Analysis of OncoPPi connectivity (protein-protein interaction network of cancer-associated genes) identified MAP kinase kinase 3 was (MKK3) as one of the major hub proteins in the network. MMK3 regulates cellular growth through phosphorylation of p38 and its activation of MYC through PPI.
CTD2 scientists at UT Southwestern identify human KRAS and loss of LKB1 lung tumors share metabolic signatures of perturbed nitrogen handling. This genotype imposes a metabolic vulnerability related to a dependence on pyrimidine metabolism in an aggressive subset of NSCLC.
CTD2 investigators at DFCI identified genes required for the survival of cancer cells in the presence of PI3K inhibition using genome-scale shRNA-based apoptosis screens.
CTD2 researchers report improved interpretability of the EDDY-CTRP results by using STITCH (protein) and STRING (drug)-interaction databases to generate evidence networks of drug-mediator pairs. These evidence networks will provide insights to drug sensitivity.