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Hypermethylation of the suppressor of cytokine signalling‐1 (SOCS‐1) in myelodysplastic syndrome
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| Zeitschriftentitel: | British Journal of Haematology |
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| Personen und Körperschaften: | , , , , |
| In: | British Journal of Haematology, 130, 2005, 2, S. 209-217 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Wiley
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| Schlagwörter: |
| Zusammenfassung: | <jats:title>Summary</jats:title><jats:p>Transcriptional silencing because of hypermethylation is now recognised to be a hallmark of human tumours. In contrast to acute myeloid leukaemia (AML), comparably little is known about aberrant methylation in myelodysplastic syndrome (MDS), a heterogeneous clonal stem cell disorder with a risk of transformation into secondary AML of up to 30%. Recent evidence demonstrates that suppressor of cytokine signalling <jats:italic>SOCS‐1</jats:italic>, a negative regulator of cytokine pathways, may act as a tumour suppressor gene, and inactivation because of hypermethylation was shown in various malignancies. Employing a newly developed quantitative real‐time polymerase chain reaction‐based methylation assay we analysed, for the first time, <jats:italic>SOCS‐1</jats:italic> methylation in MDS and found disease‐specific hypermethylation in 27 of 86 MDS patients (31%). Demethylation experiments provided direct evidence that aberrant methylation of <jats:italic>SOCS‐1</jats:italic> induces transcriptional silencing in myeloid cells. In addition, by analysing the expression of signal transducers and activators of transcription (STAT)‐induced genes we provide for the first time evidence that the activity of the Janus kinase/STAT pathway is increased in primary patient samples showing <jats:italic>SOCS‐1</jats:italic> hypermethylation.</jats:p> |
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| Umfang: | 209-217 |
| ISSN: |
0007-1048
1365-2141 |
| DOI: | 10.1111/j.1365-2141.2005.05590.x |