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Thrombocytosis and STAT5 activation in chronic myelogenous leukaemia are not associated with JAK2 V617F or calreticulin mutations
  1. Samir K Turakhia,
  2. Gurunathan Murugesan,
  3. Claudiu V Cotta,
  4. Karl S Theil
  1. Department of Laboratory Medicine, Robert J. Tomsich Pathology and Laboratory Medicine Institute, Cleveland Clinic, Cleveland, Ohio, USA
  1. Correspondence to Dr Claudiu V Cotta, Cleveland Clinic, 9500 Euclid Avenue/L-30, Cleveland, OH 44195 USA; cottac{at}ccf.org

Abstract

Aims Marked thrombocytosis is uncommon in chronic myelogenous leukaemia (CML) but may be associated with mutation of JAK2 V617F, calreticulin (CALR) and/or phospho-STAT5 (p-STAT5) activation in other myeloproliferative neoplasms (MPNs), particularly essential thrombocythaemia (ET). We investigated the JAK2 V617F, CALR and STAT5 activation status in patients with CML and thrombocytosis (CML-T) that mimicked ET, trying to identify a common mechanism for thrombocytosis in MPN.

Methods Blood and bone marrow morphological findings were reviewed from seven CML-T, four otherwise typical CML and one CML in blast phase. All cases were analysed for BCR-ABL1, JAK2 V617F and CALR exon 9 mutation and p-STAT5 expression.

Results Four of seven cases of CML-T had marked thrombocytosis (>1000×109/L). Eleven of 12 cases had megakaryocyte morphology typical for CML. All cases were BCR-ABL1 positive. Eleven of 12 cases were negative for JAK2 V617F, while STAT5 was activated in six of seven CML-T and in four of five CML cases. No case had a detectable CALR exon 9 mutation. One case of CML developed ET-like morphology and had JAK2 V617F detected while in molecular remission for CML.

Conclusions Detection of BCR-ABL1 is critical in the distinction of ET from CML. Thrombocytosis and STAT5 activation in CML-T are not consistently associated with CALR exon 9 or JAK2 V617F mutation.

  • CHRONIC MYELOID LEUKAEMIA
  • CYTOGENETICS
  • HAEMATOPATHOLOGY
  • MYELOPROLIFERATIVE DISEASE
  • THROMBOCYTHAEMIA

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