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
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.
TARGET researchers perform the first comprehensive genomic study of T-lineage acute lymphoblastic leukemia (T-ALL) and identify a large number of unrecognized driver mutations in targetable pathways. These results have significant therapeutic weight in children with T-ALL.
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.
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 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.
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.
Review on the emerging paradigm of reactive oxygen species function as specific, intracellular secondary messengers rather than as binary, indiscriminate, damaging molecules in cancer.
CTD2 researchers at Dana Farber Cancer Institute identify genome editing by CRISPR-Cas9 and gene suppression by CRISPRi have different off-target effects and combining these approaches provides complementary information in loss-of-function genetic screens.
Researchers characterized the role of the transcription repressor ZBTB18 as a putative tumor suppressor in mesenchymal subtype of glioblastoma.