* denotes a publication that resulted from CTD2 intra-Network collaborations
CTD2 scientists at DFCI systematically analyzed loss-of-function screens in cancer cell lines combined with TP53 mutagenesis screens. These studies determined the function of every possible missense or nonsense TP53 mutations and have shown increased cell proliferation.
CTD2 scientists demonstrated that the myoepithelial cells block luminal epithelial cell dispersal. This depends on the smooth muscle contractility and adhesion.
Integration of functional proteomics, systems biology, and molecular biology studies identified mTORC1 functions as a mediator between nutrition availability sensing and determinant for G2/M checkpoint recovery.
High-throughput functional siRNA screening in ovarian cancer cell lines identified that tyrosine kinase with immunoglobulin-like and EGF-like domains 1, TIE-1 confers resistance to cisplatin and could be a potential therapeutic target for platinum resistant ovarian cancer.
Studies conducted by CTD2 scientists at Oregon Health and Science University have shown that combined inhibition of JAK1/2 and BCL2 as a potential therapeutic option for acute myeloid leukemia (AML) patients.
CTD2 researchers at UCSF showed that SHP2, a non-receptor protein tyrosine phosphatase, could be a potential molecular target in cancers driven by oncogenic mutants of RAS/MAPK pathway.