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The role of histone protein modifications and mutations in histone modifiers in pediatric b-cell progenitor acute lymphoblastic leukemia

  • Szymon Janczar(corresponding author)
    ,
  • Karolina Janczar
    ,
  • Agata Pastorczak
    ,
  • Hani Harb
    ,
  • Adam J.W. Paige
    ,
  • Beata Zalewska-Szewczyk
*Corresponding author for this work
  • Medical University of Łódź
    ,
  • University of Marburg
Research Output:
Contribution to journal
Review article
 Peer-review

Open access

Sustainable Development Goals

  • SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well

Abstract

While cancer has been long recognized as a disease of the genome, the importance of epigenetic mechanisms in neoplasia was acknowledged more recently. The most active epigenetic marks are DNA methylation and histone protein modifications and they are involved in basic biological phenomena in every cell. Their role in tumorigenesis is stressed by recent unbiased large-scale studies providing evidence that several epigenetic modifiers are recurrently mutated or frequently dysregulated in multiple cancers. The interest in epigenetic marks is especially due to the fact that they are potentially reversible and thus druggable. In B-cell progenitor acute lymphoblastic leukemia (BCP-ALL) there is a relative paucity of reports on the role of histone protein modifications (acetylation, methylation, phosphorylation) as compared to acute myeloid leukemia, T-cell ALL, or other hematologic cancers, and in this setting chromatin modifications are relatively less well studied and reviewed than DNA methylation. In this paper, we discuss the biomarker associations and evidence for a driver role of dysregulated global and loci-specific histone marks, as well as mutations in epigenetic modifiers in BCP-ALL. Examples of chromatin modifiers recurrently mutated/disrupted in BCP-ALL and associated with disease outcomes include MLL1, CREBBP, NSD2, and SETD2. Altered histone marks and histone modifiers and readers may play a particular role in disease chemoresistance and relapse. We also suggest that epigenetic regulation of B-cell differentiation may have parallel roles in leukemogenesis.

Publication Information

Output type

Research Output:
Contribution to journal
Review article
 Peer-review

Original language

English

Article number

2

Pages from-to (Number of pages)

Pages 2

Journal (Volume, Issue Number)

Cancers (Volume 9, Issue 1)

Publication milestones

  • Accepted/In press - 23/12/2016
  • Published - 03/01/2017

Publication status

Published - 03/01/2017

Publication IDs

  • handle.net: 10547/623158
  • Scopus: 85009821235

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