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. 2020 Jan 28;9(2):309. doi: 10.3390/cells9020309

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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According to PanIN and IPMN stage, a time-manner dependent accumulation of point mutations in oncogenes and tumor suppressor genes, epigenetic alterations and chromosomal structural variants are represented. Furthermore, PC is mainly represented by desmoplastic stroma and immunosuppressive TME: indeed, cell populations, collagen organization, and cytokines are profoundly different between normal pancreatic tissue and advanced PC. DC, dendritic cells; GNAS, guanine nucleotide binding protein, alpha stimulating; IPMN, intraductal papillary mucinous neoplasm; KRAS, Kirsten rat sarcoma; MDSC, myeloid-derived suppressor cells; PanIN, pancreatic intraepithelial lesion; PC, pancreatic cancer; PDAC, pancreatic ductal adenocarcinoma; PSC, pancreatic stellate cells; TME, tumor microenvironment; TP53, tumor suppressor protein 53.