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. 2019 Dec 19;12(1):19. doi: 10.3390/cancers12010019

Figure 2.

Figure 2

The role of Janus kinase 1 (JAK1)/STAT3 signaling in DLBCL. In ABC DLBCL, JAK1 and STAT3 are constitutively activated by autocrine production of IL-6 and/or IL-10 as a result of MYD88 mutations (mainly L265P) and other NF-κB activation mechanisms. Constitutive activation of JAK1 and STAT3 promotes cell survival and proliferation, modulates the tumor microenvironment and promotes tumor immune evasion through the canonical STAT3 pathway as well as the noncanonical chromatin modification mechanism by JAK1 (see details in the text).