In This Issue
Cancer Discov April 1 2017 7 (4) 339-341; DOI:10.1158/2159-8290.CD-ITI7-4
In-depth genetic characterization of the genomic landscape of hepatosplenic T-cell lymphoma identifies SETD2 as a tumor suppressor and STAT5B and PIK3CD as drivers of hepatosplenic T-cell lymphoma.
PTEN-mutant tumor cells require glutamine-dependent de novo pyrimidine synthesis for their enhanced proliferation and survival, creating a vulnerability that may be targeted with DHODH inhibitors to induce DNA damage and cell death.
Chemotherapy activates the de novo pyrimidine synthesis pathway to elevate pyrimidine nucleotide levels in TNBC, suggesting that targeting de novo pyrimidine synthesis may enhance chemotherapeutic efficacy.
The multikinase inhibitor entrectinib is well tolerated and has antitumor activity in patients with TKI-naïve NTRK1/2/3, ROS1, or ALK-rearranged tumors, including those with CNS disease.
A pan-cancer genome-wide association study of data from The Cancer Genome Atlas identifies genetic risk variants that affect cancer-specific somatic alterations and influence tumor site of origin.
The putative tumor suppressor FZR1 negatively regulates BRAF kinase activity via APC/C-dependent ubiquitination and subsequent proteolysis in nontransformed cells and APC/Cindependent disruption of BRAF dimerization in cancer cells.