Figure 4 Oncogenic KRAS and inflammation

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Figure 4 Oncogenic KRAS and inflammation as drivers of acinar-to-ductal metaplasia and clonal expansion Figure 4 | Oncogenic KRAS and inflammation as drivers of acinar-to-ductal metaplasia and clonal expansion. Schematic showing how macrophage subtypes and genetic mutations contribute to acinar-to-ductal metaplasia (ADM), clonal expansion and progression to pancreatic cancer. During pancreatitis ADM is a reversible process, but becomes irreversible when an oncogenic Kras mutation is present. The accumulation of KRAS activity as caused by oncogenic Kras mutations and epidermal growth factor receptor (EGFR)–wild-type KRAS signalling, as well as loss of senescence due to an additional inactivation of cyclin-dependent kinase inhibitor 2A (CDKN2A, also known as p16INK1A), is needed for progression. Further progression to pancreatic intraepithelial neoplasia (PanIN)-2, carcinoma in situ (PanIN3) and pancreatic ductal adenocarcinoma (PDAC) occurs after acquisition of additional gene mutations in Tp53 (p53), Brca2 and Smad4. The progression to cancerous lesions occurs with an increase in desmoplasia. Cells positive for the serine/threonine-protein kinase DCLK1 are of acinar origin, are formed mainly in low-grade PanIN lesions (PanIN1A, PanIN1B and PanIN2) and have cancer stem cell functions. Storz, P. (2017) Acinar cell plasticity and development of pancreatic ductal adenocarcinoma Nat. Rev. Gastroenterol. Hepatol. doi:10.1038/nrgastro.2017.12