In This Issue
Cancer Discov July 1 2019 9 (7) 813-816; DOI:10.1158/2159-8290.CD-ITI9-7
Organoids derived from head and neck squamous cell carcinoma (HNSCC) and matching normal tissue allow for the in vitro characterization of the genetics, histology, and drug sensitivity of HNSCC.
Analysis of a long-term primary acute myeloid leukemia (AML) ex vivo culture platform shows that combined targeting of enhancers with an LSD1 inhibitor and promoters with 5-azacytidine shows greater efficacy than monotherapy, particularly in TET2-mutant AML.
Depletion of mitochondrial proteins involved in maintenance of mitochondrial function and structure including the chaperonin CLPB is synthetically lethal with venetoclax in acute myeloid leukemia cells.
Inactivation of p53 and proapoptotic proteins promotes resistance to venetoclax in acute myeloid leukemia by inducing changes in mitochondrial homeostasis and cellular metabolism.
An allosteric inhibitor of mutant EGFR is effective against common resistance mutations alone or in combination with mutant-selective ATP-competitive EGFR inhibitors.
Analysis of in vivo models of double-hit lymphoma reveals the molecular mechanism underlying the role of cyclophosphamide and other alkylating agents on tumor clearance and antibody resistance.
The gain-of-function mutant p53R172H upregulates the transcription factor FOXH1 to promote self-renewal in acute myeloid leukemia.