SOCS2 is dispensable for BCR/ABL1-induced chronic myeloid leukemia-like disease and for normal hematopoietic stem cell function
- Author(s)
- Hansen, N; Agerstam, H; Wahlestedt, M; Landberg, N; Askmyr, M; Ehinger, M; Rissler, M; Lilljebjorn, H; Johnels, P; Ishiko, J; Melo, JV; Alexander, WS; Bryder, D; Jaras, M; Fioretos, T;
- Details
- Publication Year 2013-01,Volume 27,Issue #1,Page 130-135
- Journal Title
- LEUKEMIA
- Publication Type
- Journal Article
- 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 (2013) 27, 130-135; doi:10.1038/leu.2012.169
- Publisher
- NATURE PUBLISHING GROUP
- Keywords
- CHRONIC MYELOGENOUS LEUKEMIA; BCR-ABL; CYTOKINE SIGNALING-2; TYROSINE PHOSPHORYLATION; FAMILY-MEMBERS; ALOX5 GENE; EXPRESSION; MICE; SUPPRESSOR; GROWTH
- Research Division(s)
- Cancer And Haematology
- Link To PubMed Central Version
- http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3542906/
- Publisher's Version
- https://doi.org/10.1038/leu.2012.169
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Creation Date: 2013-01-01 12:00:00