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Genomic abnormalities as biomarkers and therapeutic targets in acute myeloid leukaemia
File(s)
cancers-13-05055-v2.pdf (1.06 MB)
Published version
Author(s)
Ribeiro, Sara
Eiring, Anna
Sorouri Khorashad, J
Type
Journal Article
Abstract
Acute myeloid leukemia (AML) is a highly heterogeneous malignancy characterized by the clonal expansion of myeloid stem and progenitor cells in the bone marrow, peripheral blood, and other tissues. AML results from the acquisition of gene mutations or chromosomal abnormalities that induce proliferation or block differentiation of hematopoietic progenitors. A combination of cytogenetic profiling and gene mutation analyses are essential for the proper diagnosis, classification, prognosis, and treatment of AML. In the present review, we provide a summary of genomic abnormalities in AML that have emerged as both markers of disease and therapeutic targets. We discuss the abnormalities of RARA, FLT3, BCL2, IDH1, and IDH2, their significance as therapeutic targets in AML, and how various mechanisms cause resistance to the currently FDA-approved inhibitors. We also discuss the limitations of current genomic approaches for producing a comprehensive picture of the activated signaling pathways at diagnosis or at relapse in AML patients, and how innovative technologies combining genomic and functional methods will improve the discovery of novel therapeutic targets in AML. The ultimate goal is to optimize a personalized medicine approach for AML patients and possibly those with other types of cancers.
Date Issued
2021-10-09
Date Acceptance
2021-10-08
Citation
Cancers, 2021, 13 (20), pp.1-21
URI
URL
DOI
ISSN
2072-6694
Publisher
MDPI AG
Start Page
1
End Page
21
Journal / Book Title
Cancers
Volume
13
Issue
20
Copyright Statement
© 2021 by the authors.
Licensee MDPI, Basel, Switzerland.
This article is an open access article
distributed under the terms and
conditions of the Creative Commons
Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
License URL
Sponsor
Leuka
Identifier
https://www.mdpi.com/2072-6694/13/20/5055
Grant Number
N/A
Subjects
1112 Oncology and Carcinogenesis
Publication Status
Published
Date Publish Online
2021-10-09