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

Hansen, Nils LU ; Ågerstam, Helena LU ; Wahlestedt, Martin LU ; Landberg, Niklas LU ; Askmyr, Maria LU ; Ehinger, Mats LU ; Rissler, Marianne LU ; Lilljebjörn, Henrik LU ; Johnels, Petra LU and Ishiko, J, et al. (2013) In Leukemia 27. p.130-135
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... (More)
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. (Less)
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published
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Leukemia
volume
27
pages
130 - 135
publisher
Nature Publishing Group
external identifiers
  • wos:000313511400018
  • pmid:22824785
  • scopus:84873569948
ISSN
1476-5551
DOI
10.1038/leu.2012.169
language
English
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yes
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0608cdce-1f6a-4ed6-9a64-297fcce6daf2 (old id 2966743)
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http://www.ncbi.nlm.nih.gov/pubmed/22824785?dopt=Abstract
date added to LUP
2012-08-09 21:14:00
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2019-03-13 10:30:45
@article{0608cdce-1f6a-4ed6-9a64-297fcce6daf2,
  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.},
  author       = {Hansen, Nils and Ågerstam, Helena and Wahlestedt, Martin and Landberg, Niklas and Askmyr, Maria and Ehinger, Mats and Rissler, Marianne and Lilljebjörn, Henrik and Johnels, Petra and Ishiko, J and Melo, J V and Whalen, Alexander and Bryder, David and Järås, Marcus and Fioretos, Thoas},
  issn         = {1476-5551},
  language     = {eng},
  pages        = {130--135},
  publisher    = {Nature Publishing Group},
  series       = {Leukemia},
  title        = {SOCS2 is dispensable for BCR/ABL1-induced chronic myeloid leukemia-like disease and for normal hematopoietic stem cell function.},
  url          = {http://dx.doi.org/10.1038/leu.2012.169},
  volume       = {27},
  year         = {2013},
}