Deoxyribonucleic acid methylation driven aberrations in pancreatic cancer-related pathways

Figure 1 Comprehensive visualization showcasing interaction between epigenetic pathways and probable drug treatments concerning pancreatic cancer. EGF: Epidermal growth factor; Ras/Raf/MEK/ERK: Rat sarcoma virus/Rapidly Accelerated Fibrosarcoma/Mitogen-activated protein kinase/extracellular-signal-regulated kinase; PI3K/AKT/mTOR: Phosphoinositide 3-kinases/Ak strain transforming/Mammalian target of rapamycin; Wnt: Wingless-related integration site; PDGF: Platelet-derived growth factor; SCF/c-Kit: Stem cell factor/receptor tyrosine kinase; ALK: Anaplastic lymphoma kinase; TGF-β: Transforming growth factor beta; HGF: Hepatocyte growth factor; JAK/STAT: Janus kinase/signal transducers and activators of transcription; BTK: Bruton tyrosine kinase; Src: Tyrosine-protein kinase (sarcoma); COX-2: Cyclooxygenase 2; NRF2: Nuclear factor erythroid 2–related factor 2; HIF-1: Hypoxia-inducible factor-1; PKCδ-PKD1: Protein Kinase Cδ-Polycystin 1, Transient Receptor Potential Channel Interacting; IGF: Insulin like growth factor; VEGF: Vascular endothelial growth factor.