Recent advances in targeted therapy for pancreatic adenocarcinoma

Figure 1 Overview of targeted therapy strategies for pancreatic adenocarcinoma. The figure summarizes the systemic therapeutic targets and corresponding drugs for pancreatic cancer, including treatment strategies for many aspects such as signaling pathways and gene mutations in tumor cells, and molecules in the extracellular environment, and extracellular matrix. “—|” indicates “targeting”; Akt: Akt serine/threonine kinase; BTK: Bruton’s tyrosine kinase; CDK4/6: Cyclin-dependent kinase 4/6; CSC: Cancer stem cell; CTGF: Connective tissue growth factor; DC: Dendritic cell; EGFR: Epidermal growth factor receptor; ERK: Extracellular-regulated protein kinase; HGF: Hepatocyte growth factor; IGF-1R: Insulin-like growth factor receptor; JAK: Activation of the Janus kinase; KRAS: Kirsten rat sarcoma oncogene; MEK: Mitogen-activated protein kinase; MMP: Matrix metalloproteinase; mTOR: Mammalian target of rapamycin; Notch: Notch receptor; PARP: Poly (ADP-ribose) polymerase; NRG1: Neuregulin 1; NTRK: Neurotrophic receptor tyrosine kinase; PEGPH20: Pegylated recombinant human hyaluronidase PH20; PI3K: Phosphatidylinositol 3-kinase; PSC: Pancreatic stellate cell; RAF: Rapid accelerated fibrosarcoma; SMAD4: Mothers against decapentaplegic homolog 4; SHH: Sonic hedgehog pathway; SMO: Smoothened; STAT: Signal transducer and transcription; TGF-β: Transforming growth factor-β; VEGFR: Vascular endothelial growth factor receptor.