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SOCS2 is dispensable for BCR/ABL1-induced chronic myeloid leukemia-like disease and for normal hematopoietic stem cell function.

  • Nils Hansen
  • Helena Ågerstam
  • Martin Wahlestedt
  • Niklas Landberg
  • Maria Askmyr
  • Mats Ehinger
  • Marianne Rissler
  • Henrik Lilljebjörn
  • Petra Johnels
  • J Ishiko
  • J V Melo
  • Alexander Whalen
  • David Bryder
  • Marcus Järås
  • Thoas Fioretos
Publishing year: 2013
Language: English
Pages: 130-135
Publication/Series: Leukemia
Volume: 27
Document type: Journal article
Publisher: Nature Publishing Group

Abstract english

Suppressor of cytokine signaling 2 (SOCS2) is known as a feedback inhibitor of cytokine signaling and is highly expressed in primary bone marrow (BM) cells from patients with chronic myeloid leukemia (CML). However, it has not been established whether SOCS2 is involved in CML, caused by the BCR/ABL1 fusion gene, or important for normal hematopoietic stem cell (HSC) function. In this study, we demonstrate that although Socs2 was found to be preferentially expressed in long-term HSCs, Socs2-deficient HSCs were indistinguishable from wild-type HSCs when challenged in competitive BM transplantation experiments. Furthermore, by using a retroviral BCR/ABL1-induced mouse model of CML, we demonstrate that SOCS2 is dispensable for the induction and propagation of the disease, suggesting that the SOCS2-mediated feedback regulation of the JAK/STAT pathway is deficient in BCR/ABL1-induced CML.Leukemia advance online publication, 24 July 2012; doi:10.1038/leu.2012.169.


  • Cancer and Oncology


  • ISSN: 1476-5551
Thoas Fioretos
E-mail: thoas.fioretos [at]

Principal investigator

Division of Clinical Genetics

+46 46 222 45 95

+46 70 334 33 67