fig1

Figure 1. The interrelationships among JAK/STAT, NF-κB, MAPK, and AKT carcinogenic pathways and dysregulated tumor suppressor genes, somatic mutations, and epigenetic mutations. Molecules located at junctions of the non-arrow ends have effects on the part pointed by the arrows. Specific explanations are disclosed in the corresponding sections. JAK/STAT: Janus kinase/signal transduction and activator of transcription; JAK2/3: Janus kinase2/3; STAT3: signal transduction and activator of transcription 3; PTPRK: receptor-type tyrosine-protein phosphatase κ; PDL1: programmed death ligand-1; NK-κB: nuclear factor kappaB; TRAF6: tumor necrosis factor receptor associated factor 6; DDX3X: DEAD-box helicase 3 X-linked; MAPK: mitogen-activated protein kinase; MAP3K6: mitogen-activated protein kinase kinase kinase 6; PRDM1: PR/SET domain 1; MYC: bHLH transcription factor; SNHG12: small nucleolar RNA host gene 12; TET1: methylcytosine dioxygenase ten-eleven translocation 1; RUNX3: runt-related transcription factor 3; EZH2: enhancer of zeste homolog 2; BCYRN1: brain cytoplasmic RNA 1; AKT: protein kinase B.