Emerging therapies for inv(16) AML. Blood 2021 May 13;137(19):2579-2584
Date
04/07/2021Pubmed ID
33821975Pubmed Central ID
PMC8120144DOI
10.1182/blood.2020009933Scopus ID
2-s2.0-85105729513 (requires institutional sign-in at Scopus site) 13 CitationsAbstract
The core binding factor composed of CBFβ and RUNX subunits plays a critical role in most hematopoietic lineages and is deregulated in acute myeloid leukemia (AML). The fusion oncogene CBFβ-SMMHC expressed in AML with the chromosome inversion inv(16)(p13q22) acts as a driver oncogene in hematopoietic stem cells and induces AML. This review focuses on novel insights regarding the molecular mechanisms involved in CBFβ-SMMHC-driven leukemogenesis and recent advances in therapeutic approaches to target CBFβ-SMMHC in inv(16) AML.
Author List
Surapally S, Tenen DG, Pulikkan JAAuthor
John A. Pulikkan PhD Assistant Professor in the Cell Biology, Neurobiology and Anatomy department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsAntineoplastic Agents, Immunological
Antineoplastic Combined Chemotherapy Protocols
Cell Transformation, Neoplastic
Chromosome Inversion
Chromosomes, Human, Pair 16
Combined Modality Therapy
Core Binding Factor Alpha 2 Subunit
Core Binding Factor beta Subunit
Forecasting
Gene Expression Regulation, Leukemic
Gene Knock-In Techniques
Hematopoiesis
Humans
Immunotherapy
Leukemia, Myeloid, Acute
Mice
Molecular Targeted Therapy
Myosin Heavy Chains
Neoplastic Stem Cells
Oncogene Proteins, Fusion
T-Lymphocytes
Xenograft Model Antitumor Assays
