Article Text

Download PDFPDF
Letter to the editor
GATA1 mutations are not a hallmark of acute myeloid leukaemia with t(8;21)
  1. Sylvia Hoeller1,
  2. Michel P Bihl1,
  3. Caroline Arber2,
  4. Stephan Dirnhofer1,
  5. Alexandar Tzankov1
  1. 1Institute of Pathology, University Hospital Basel, University of Basel, Basel, Switzerland
  2. 2Department of Haematology, University Hospital Basel, University of Basel, Basel, Switzerland
  1. Correspondence to Alexandar Tzankov, Institute of Pathology, Schoenbeinstrasse 40, Basel CH-4031, Switzerland; atzankov{at}

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

Leukaemogenesis is a stepwise process of a delimited number of genetic aberrations, which lead to maturation impairment and promote proliferation and/or survival of the neoplastic clone.1 In acute myeloid leukaemia (AML) with t(8;21)(q22;q22)/RUNX1-RUNX1T1, genetic aberrations additional to the core-binding factor rearrangement are well known.2 Presumably further aberrations are also involved in leukaemogenesis of such AML, but are yet to be discovered.

Decrease/loss of function of the transcription factor GATA1 plays a central role in transient myeloproliferative disorders (TMDs) of newborns with trisomy 21.3–6 The presence of a short protein isoform, generated by a mutation, is complementary to trisomy 21 to initiate TMD.6 7 Since the potent oncogene RUNX1 is located …

View Full Text


  • Competing interests None.

  • Provenance and peer review Not commissioned; externally peer reviewed.