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Despite the recent emergence of novel chemotherapy regimen such as nab-paclitaxel/gemcitabine and FOLFIRINOX (folinic acid, fluorouracil, irinotecan and oxaliplatin), pancreatic ductal adenocarcinoma (PDA) is characterised by a poor response to chemotherapy and radiotherapy. Therefore, it remains a challenge for clinicians and scientists likewise to overcome resistance to treatment. PDA silently develops from preneoplastic lesions (PanINs I–III) to invasive cancer over a long period of time. A number of genetic mutations have been identified and well characterised during the evolution of PDA, such as the Kras oncogene, and tumour suppressor genes p16, p53 and DPC4. In addition to genetic mutations, epigenetic modifications and complex alterations within the tumour microenvironment give rise to cell autonomous and non-cell autonomous mechanisms of therapy resistance. Over the past years, it has emerged that therapeutic resistance is, at least in part, mediated by cancer stem cells (CSCs) that are perpetuated within a small fraction of cells within the tumour bulk.1 Stemness and epithelial to mesenchymal transition are closely related on a molecular level and …
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