Low burden of a JAK2-V617F mutated clone in monoclonal haematopoiesis in a Japanese woman with Budd-Chiari syndrome

Int J Hematol. 2009 May;89(4):517-522. doi: 10.1007/s12185-009-0280-y. Epub 2009 Mar 24.

Abstract

Approximately one-half of the cases of Budd-Chiari syndrome (BCS) are caused by bcr/abl negative chronic myeloproliferative disorders (CMPDs). Furthermore, a mutation in the Janus kinase protein (JAK2-V617F) is detected in half of the patients with BCS. However, whether the JAK2 mutation is the primary event leading to CMPDs and BCS is controversial. We present a report concerning a young woman who suffered from BCS prior to the onset of CMPDs. Analysis of X-chromosome inactivation patterns in this patient, using the human androgen receptor gene demonstrated monoclonal haematopoiesis in her granulocytes. In contrast, she had a low burden of a JAK2-V617F mutation positive clone among granulocyte populations. These results suggest that the JAK2-V617F mutation occurs after the onset of monoclonal haematopoiesis; thus the V617F mutation of JAK2 may not be the primary event in the induction of BCS.

Publication types

  • Case Reports

MeSH terms

  • Adult
  • Asian People / genetics*
  • Base Sequence
  • Budd-Chiari Syndrome / diagnostic imaging
  • Budd-Chiari Syndrome / enzymology*
  • Budd-Chiari Syndrome / genetics
  • Budd-Chiari Syndrome / pathology
  • DNA / genetics
  • Female
  • Genome, Human / genetics
  • Hematopoiesis / genetics*
  • Humans
  • Janus Kinase 2 / genetics*
  • Janus Kinase 2 / metabolism*
  • Mutation / genetics
  • Phenylalanine / genetics
  • Phenylalanine / metabolism
  • RNA / genetics
  • Tomography, X-Ray Computed
  • Valine / genetics
  • Valine / metabolism
  • X Chromosome Inactivation / genetics

Substances

  • Phenylalanine
  • RNA
  • DNA
  • Janus Kinase 2
  • Valine