Chromosomal Instability in Acute Myeloid Leukemia

Chromosomal instability (CIN), the increasing rate in which cells acquire new chromosomal alterations, is one of the hallmarks of cancer. Many studies highlighted CIN as an important mechanism in the origin, progression, and relapse of acute myeloid leukemia (AML). The ambivalent feature of CIN as a...

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Published inCancers Vol. 13; no. 11; p. 2655
Main Authors de Oliveira Lisboa, Mateus, Brofman, Paulo Roberto Slud, Schmid-Braz, Ana Teresa, Rangel-Pozzo, Aline, Mai, Sabine
Format Journal Article
LanguageEnglish
Published Basel MDPI AG 28.05.2021
MDPI
Subjects
Acute myeloid leukemia
Age
aneuploidy
Apoptosis
Blood diseases
Cancer
Cell cycle
Cell death
Cell division
chromosomal instability
Chromosomes
complex karyotype
cytogenetic heterogeneity
Cytogenetics
Evolution
Genes
Genetic diversity
Genomic instability
Leukemia
Mutation
Myeloid leukemia
Proteins
Review
Therapeutic targets
TP53
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Summary:Chromosomal instability (CIN), the increasing rate in which cells acquire new chromosomal alterations, is one of the hallmarks of cancer. Many studies highlighted CIN as an important mechanism in the origin, progression, and relapse of acute myeloid leukemia (AML). The ambivalent feature of CIN as a cancer-promoting or cancer-suppressing mechanism might explain the prognostic variability. The latter, however, is described in very few studies. This review highlights the important CIN mechanisms in AML, showing that CIN signatures can occur largely in all the three major AML types (de novo AML, secondary-AML, and therapy-related-AML). CIN features in AML could also be age-related and reflect the heterogeneity of the disease. Although most of these abnormalities show an adverse prognostic value, they also offer a strong new perspective on personalized therapy approaches, which goes beyond assessing CIN in vitro in patient tumor samples to predict prognosis. Current and emerging AML therapies are exploring CIN to improve AML treatment, which includes blocking CIN or increasing CIN beyond the limit threshold to induce cell death. We argue that the characterization of CIN features, not included yet in the routine diagnostic of AML patients, might provide a better stratification of patients and be extended to a more personalized therapeutic approach.
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ISSN:2072-6694
2072-6694
DOI:10.3390/cancers13112655