Epigenetic dysregulation of the Jak/STAT pathway by frequent aberrant methylation of SHP1 but not SOCS1 in acute leukaemias
Epigenetic dysregulation of the Jak/STAT pathway by frequent aberrant methylation of SHP1 but not SOCS1 in acute leukaemias
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DOI：
10.1007/s00277-004-0843-1
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发表时间：
2004-08-01
影响因子：
3.5
通讯作者：
Kwong, YL
中科院分区：
文献类型：
--
作者：
Chim, CS;Wong, ASY;Kwong, YL
SOCS 1和SHP 1是与白血病发生有关的Jak/STAT信号通路的负调节因子。我们应用甲基化特异性聚合酶链反应（MSP）研究SOCS 1和SHP 1基因的异常甲基化是否参与了急性白血病的发病和预后。在诊断时，急性髓性白血病（AML）（n=26，52%）比急性淋巴细胞白血病（ALL）（n=6，24%）更频繁地发生SHP 1甲基化（p=0.02）。AML和ALL患者中SOCS 1均不存在甲基化。SHP 1甲基化与特定的临床病理特征无关，对AML患者的预后无影响。SHP 1的频繁甲基化，而不是SOCS 1，可能在急性白血病的发病机制中很重要，但不是预后。
SOCS1 and SHP1 are negative regulators of the Jak/STAT signalling pathway that is implicated in leukaemogenesis. We studied if aberrant methylation of SOCS1 and SHP1 might be involved in the pathogenesis and prognostication of acute leukaemias by methylation-specific polymerase chain reaction (MSP). At diagnosis, methylation of SHP1 occurred more frequently in acute myeloid leukaemia (AML) (n=26, 52%) than acute lymphoblastic leukaemia (ALL) (n=6, 24%) (p=0.02). Methylation of SOCS1 was absent in both AML and ALL patients. SHP1 methylation was not associated with specific clinicopathologic features and had no prognostic impact on AML patients. Frequent methylation of SHP1, but not SOCS1, may be important in the pathogenesis, but not prognosis, of acute leukaemias.