SOCS2 is dispensable for BCR/ABL1-induced chronic myeloid leukemia-like disease and for normal hematopoietic stem cell function.
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/2966743
- author
- organization
-
- Division of Clinical Genetics
- Department of Experimental Medical Science
- Tumor microenvironment
- Family Medicine and Clinical Epidemiology (research group)
- StemTherapy: National Initiative on Stem Cells for Regenerative Therapy
- BioCARE: Biomarkers in Cancer Medicine improving Health Care, Education and Innovation
- publishing date
- 2013
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Leukemia
- volume
- 27
- pages
- 6 pages
- publisher
- Nature Publishing Group
- external identifiers
-
- wos:000313511400018
- pmid:22824785
- scopus:84873569948
- pmid:22824785
- ISSN
- 1476-5551
- DOI
- 10.1038/leu.2012.169
- language
- English
- LU publication?
- yes
- additional info
- 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)
- id
- 0608cdce-1f6a-4ed6-9a64-297fcce6daf2 (old id 2966743)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/22824785?dopt=Abstract
- date added to LUP
- 2016-04-01 13:15:42
- date last changed
- 2022-04-06 03:34:48
@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 = {{https://lup.lub.lu.se/search/files/3262845/3615621.pdf}}, doi = {{10.1038/leu.2012.169}}, volume = {{27}}, year = {{2013}}, }