Format

Send to

Choose Destination
J Exp Clin Cancer Res. 2018 Feb 23;37(1):36. doi: 10.1186/s13046-018-0704-8.

CDK9 inhibitors in acute myeloid leukemia.

Author information

1
Sbarro Institute for Cancer Research and Molecular Medicine, Department of Biology, Temple University, 1900 N. 12th St., Room 431, Philadelphia, PA, 19122-6017, USA.
2
Medical Oncology Unit, Clinical Cancer Centre, IRCCS-Arcispedale S. Maria Nuova, Reggio Emilia, Italy.
3
Oncology Research Center of Mercogliano (CROM), Istituto Nazionale Per Lo Studio E La Cura Dei Tumori "Fondazione Giovanni Pascale", IRCCS, Naples, Italy.
4
Sbarro Institute for Cancer Research and Molecular Medicine, Department of Biology, Temple University, 1900 N. 12th St., Room 431, Philadelphia, PA, 19122-6017, USA. giordano@temple.edu.
5
Department of Medicine, Surgery, and Neuroscience, University of Siena, Siena, Italy. giordano@temple.edu.

Abstract

Current treatment for acute myeloid leukemia (AML) is less than optimal, but increased understanding of disease pathobiology and genomics has led to clinical investigation of novel targeted therapies and rational combinations. Targeting the cyclin-dependent kinase 9 (CDK9) pathway, which is dysregulated in AML, is an attractive approach. Inhibition of CDK9 leads to downregulation of cell survival genes regulated by super enhancers such as MCL-1, MYC, and cyclin D1. As CDK9 inhibitors are nonselective, predictive biomarkers that may help identify patients most likely to respond to CDK9 inhibitors are now being utilized, with the goal of improving efficacy and safety.

KEYWORDS:

Acute myeloid leukemia; CDK9 inhibitor; MCL-1; MYC; P-TEFb; Positive transcription elongation factor b

Supplemental Content

Full text links

Icon for BioMed Central Icon for PubMed Central
Loading ...
Support Center