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

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Abstract

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.
Original languageEnglish
Pages (from-to)130-135
Number of pages6
JournalLeukemia
Volume27
DOIs
Publication statusPublished - 2013

Bibliographical note

The information about affiliations in this record was updated in December 2015.
The record was previously connected to the following departments: Family medicine, psychiatric epidemiology and migration (013240037), Pathology, (Lund) (013030000), Stem Cell Aging (013212073), Division of Clinical Genetics (013022003)

Subject classification (UKÄ)

  • Cancer and Oncology

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