title: Inhibition of EZH2 degradation as a novel approach to overcome drug resistance in acute myeloid leukemia.
abstract: The polycomb protein enhancer of zeste homolog 2 (EZH2) may have a dual role in cancer pathogenesis acting as an oncogene or as a tumor suppressor depending on the cancer type. We recently demonstrated that proteasomal degradation of EZH2 resulting from cyclin-dependent kinase 1 (CDK1)-induced phosphorylation at Threonine (T) 487 represents a novel mechanism of drug resistance in acute myeloid leukemia (AML). Our findings suggest that restoration of EZH2 protein is a viable approach to overcome therapy resistance in AML.
authors.affiliation: Department of Medicine IV, Hematology and Oncology, University Hospital of Halle (Saale), Halle (Saale), Germany; Department of Internal Medicine V, Hematology, Oncology and Rheumatology, University Hospital of Heidelberg, Heidelberg, Germany.
authors.forename: Stefanie
authors.initials: S
authors.lastname: Göllner
authors.affiliation: Department of Medicine IV, Hematology and Oncology, University Hospital of Halle (Saale), Halle (Saale), Germany; Department of Internal Medicine V, Hematology, Oncology and Rheumatology, University Hospital of Heidelberg, Heidelberg, Germany.
authors.forename: Carsten
authors.initials: C
authors.lastname: Müller-Tidow
keywords: Acute myeloid leukemia (AML); EZH2; drug resistance; epigenetic; proteasome