SOCS2 is dispensable for BCR/ABL1-induced chronic myeloid leukemia-like disease and for normal hematopoietic stem cell function.
Författare
Summary, in 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.
Avdelning/ar
- Avdelningen för klinisk genetik
- Institutionen för experimentell medicinsk vetenskap
- Tumörmikromiljö
- Allmänmedicin och klinisk epidemiologi
- StemTherapy: National Initiative on Stem Cells for Regenerative Therapy
- BioCARE: Biomarkers in Cancer Medicine improving Health Care, Education and Innovation
Publiceringsår
2013
Språk
Engelska
Sidor
130-135
Publikation/Tidskrift/Serie
Leukemia
Volym
27
Fulltext
- Available as PDF - 757 kB
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Länkar
Dokumenttyp
Artikel i tidskrift
Förlag
Nature Publishing Group
Ämne
- Cancer and Oncology
Status
Published
Forskningsgrupp
- Family Medicine and Clinical Epidemiology
ISBN/ISSN/Övrigt
- ISSN: 1476-5551