HDAC6-an Emerging Target Against Chronic Myeloid Leukemia?

Hélène Losson1, Michael Schnekenburger1, Mario Dicato1

  • 1Laboratoire de Biologie Moléculaire et Cellulaire du Cancer, Hôpital Kirchberg 9, rue Edward Steichen, L2540 Luxembourg, Luxembourg.

Cancers
|February 5, 2020
PubMed

Insights

Histone deacetylase 6 (HDAC6) is overexpressed in chronic myeloid leukemia (CML) stem cells. Targeting HDAC6 presents a promising new therapeutic strategy for CML treatment, addressing imatinib resistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Imatinib revolutionized chronic myeloid leukemia (CML) treatment, establishing a standard of care for two decades.
  • Emerging resistance to imatinib and other tyrosine kinase inhibitors necessitates the identification of novel therapeutic targets in CML.

Purpose of the Study:

  • To review the molecular characteristics of histone deacetylase 6 (HDAC6).
  • To discuss the overexpression of HDAC6 in CML leukemic stem cells.
  • To evaluate HDAC6 as a potential therapeutic target for CML.

Main Methods:

  • Literature review of studies on HDAC6.
  • Analysis of HDAC6's role in cellular activities and its cytoplasmic localization.
  • Examination of HDAC6 expression patterns in CML.

Main Results:

  • HDAC6 plays a significant role in various cellular functions due to its cytoplasmic localization.
  • Overexpression of HDAC6 has been observed in CML leukemic stem cells.

Conclusions:

  • HDAC6's molecular properties and its overexpression in CML stem cells position it as a promising therapeutic target.
  • Targeting HDAC6 may offer a new strategy to overcome imatinib resistance in CML patients.