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How frequent is SOCS1 methylation in acute myeloid leukaemia?

et al, 2001). The results obtained by MSP and biological interpretation should be viewed with caution. However, our data and others have clearly shown that gene methylation is highly restrictive to malignant cells and is closely related to down-regulation or loss of expression. With regard to SOCS-1 methylation, SOCS-1 mRNA is clearly induced by interferon-c and there have been no observations relating to the presence of frequency of promoter methylation, as discussed in our original report. Demethylating agents enable us to evaluate the role of DNA methylation in gene silencing. However, they also exert nonspecific effects that do not involve DNA methyltransferase activity. For instance, SOCS-3, which shows the highest homology to SOCS-1 among the SOCS family, was also induced by demethylating agents in some SOCS-1 methylated cell lines (Jurkat, THP-1, and U937). However, bisulphite sequencing methods of the 5¢ UTR of the SOCS-3 gene demonstrated that the SOCS-3 gene was not methylated in these cell lines (unpublished data). In contrast, some cell lines, such as Ramos and Daudi, showed loss of SOCS-3 expression and harboured 5¢ UTR methylation of SOCS-3. This observation may indicate that analysis of SOCS-1 function on the JAKSTAT pathway after treatment with demethylating agents is not possible because both SOCS-1 and SOCS-3 were restored regardless of their methylation status. Recently it was reported that short interfering RNA (siRNA) can induce targeted DNA methylation and gene silencing in human cells (Kawasaki & Taira, 2004). This finding provides a new method to investigate the role of site-specific gene methylation and silencing. Although it is not possible to create demethylation of specific sites within the cancer cell, siRNA mediated-gene methylation could evolve into a powerful tool to resolve the issues discussed here.