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CDK9 inhibitors in acute myeloid leukemia

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 dysregul...

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Detalles Bibliográficos
Autores principales: Boffo, Silvia, Damato, Angela, Alfano, Luigi, Giordano, Antonio
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5824552/
https://www.ncbi.nlm.nih.gov/pubmed/29471852
http://dx.doi.org/10.1186/s13046-018-0704-8
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author Boffo, Silvia
Damato, Angela
Alfano, Luigi
Giordano, Antonio
author_facet Boffo, Silvia
Damato, Angela
Alfano, Luigi
Giordano, Antonio
author_sort Boffo, Silvia
collection PubMed
description 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. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s13046-018-0704-8) contains supplementary material, which is available to authorized users.
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spelling pubmed-58245522018-02-26 CDK9 inhibitors in acute myeloid leukemia Boffo, Silvia Damato, Angela Alfano, Luigi Giordano, Antonio J Exp Clin Cancer Res Review 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. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s13046-018-0704-8) contains supplementary material, which is available to authorized users. BioMed Central 2018-02-23 /pmc/articles/PMC5824552/ /pubmed/29471852 http://dx.doi.org/10.1186/s13046-018-0704-8 Text en © The Author(s). 2018 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Review
Boffo, Silvia
Damato, Angela
Alfano, Luigi
Giordano, Antonio
CDK9 inhibitors in acute myeloid leukemia
title CDK9 inhibitors in acute myeloid leukemia
title_full CDK9 inhibitors in acute myeloid leukemia
title_fullStr CDK9 inhibitors in acute myeloid leukemia
title_full_unstemmed CDK9 inhibitors in acute myeloid leukemia
title_short CDK9 inhibitors in acute myeloid leukemia
title_sort cdk9 inhibitors in acute myeloid leukemia
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5824552/
https://www.ncbi.nlm.nih.gov/pubmed/29471852
http://dx.doi.org/10.1186/s13046-018-0704-8
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