| | Gene name | Related pathway | Findings in CLL | Ref. |
| | SOCS-1 | Negative regulator of type I and type II interferon and other cytokines, including IL2, IL4, IL6, and leukemia inhibitory factor; Class I MHC-mediated antigen processing and presentation; inhibitor of the JAK-STAT pathway | SOCS-1 gene body was not hypermethylated in any case | [135] | | IL19 | MIF-mediated glucocorticoid regulation, TGF-β pathway, and JAK-STAT pathway | Methylated gene body was reported in IGVH-mutated CLL cells | [26, 136] | | IFNB1 | Interferons-mediated signaling pathway DDX58/IFIH1-mediated induction of interferon-alpha/beta, JAK-STAT pathway | Methylated gene body was identified in IGVH-mutated samples | [26, 137] | | DUSP22 | Inhibitor of MAPK and STAT pathways | Silencing of DUSP22 expression in knocked-out cells resulted in increased STAT3 activity. Targeted bisulfite sequencing and methylation-specific PCR detected that the methylation levels of the DUSP22 promoter were significantly lower in DUSP22 knocked-out cells after treatment with demethylating agents, DUSP22 promoter methylation decreased and subsequently, DUSP22 mRNA levels were increased | [138] |
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CLL: chronic lymphocytic leukemia, Ref.: reference, JAK: Janus kinase, STAT: signal transducer and activator of transcription, IFNB1: interferon beta 1, IL: interleukin, SOCS-1: suppressor of cytokine signaling 1, DUSP22: dual specificity phosphatase 22, DDX58/IFIH1: DExD/H-box helicase 58/interferon induced with helicase C domain 1, MIF: macrophage migration inhibitory factor, TGF-β: transforming growth factor-beta, MHC: major histocompatibility complex, MAPK: mitogen-activated protein kinase, IGVH: immunoglobulin variable heavy chain gene.
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