disorganized. By contrast, there were no associations between IL-6/STAT3 modulation by AZA
and expression of soluble and cell surface IL-6 receptors, as well as the number or the type
mutations.
Collectively, our results demonstrate for the first time that downregulation of the IL-6/STAT3
pathway in CD4+ T cells may represent an immune-mediated mechanism of action of AZA.
The IL-6/STAT3 axis is notoriously pro-tumorigenic and pharmacologic inhibition of various
individual modules of this pathway in cancer is under development. Our findings serve as a
guidepost for the ongoing investigation of IL-6/STAT3 axis inhibition as a therapeutic strategy
to overcome AZA resistance.
