Epigenomics of leukemia: from mechanisms to therapeutic applications

Abstract

Leukemogenesis is a multistep process in which successive transformational events enhance the ability of a clonal population arising from hematopoietic progenitor cells to proliferate, differentiate and survive. Clinically and pathologically, leukemia is subdivided into four main categories: chronic lymphocytic leukemia, chronic myeloid leukemia, acute lymphocytic leukemia and acute myeloid leukemia. Leukemia has been previously considered only as a genetic disease. However, in recent years, significant advances have been made in the elucidation of the leukemogenesis-associated processes. Thus, we have come to understand that epigenetic alterations including DNA methylation, histone modifications and miRNA are involved in the permanent changes of gene expression controlling the leukemia phenotype. In this article, we will focus on the epigenetic defects associated with leukemia and their implications as biomarkers for diagnostic, prognostic and therapeutic applications.

KEYWORDS::

• cancer prevention
• DNA methylation
• epigenetic anticancer therapy
• epigenetics
• histone modifications
• leukemia
• miRNA

Financial & competing interests disclosure

This work was supported by the “Recherche Cancer et Sang” foundation, the “Recherches Scientifiques Luxembourg” association, by the “Een Häerz fir kriibskrank Kanner” association and by the Action LIONS “Vaincre le Cancer” association and by Télévie Luxembourg. Michael Schnekenburger is recipient of a Télévie Luxembourg fellowship. Cristina Florean is supported by an AFR fellowship from the Ministry of Research, Luxembourg. Publication costs were covered by the Fonds National de la Recherche Luxembourg. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

This work was supported by the “Recherche Cancer et Sang” foundation, the “Recherches Scientifiques Luxembourg” association, by the “Een Häerz fir kriibskrank Kanner” association and by the Action LIONS “Vaincre le Cancer” association and by Télévie Luxembourg. Michael Schnekenburger is recipient of a Télévie Luxembourg fellowship. Cristina Florean is supported by an AFR fellowship from the Ministry of Research, Luxembourg. Publication costs were covered by the Fonds National de la Recherche Luxembourg. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.