Metastatic Pancreatic Adenocarcinoma Perfect Paragraph

Metastatic pancreatic adenocarcinoma is driven by cancer stem cells, formation and upregulation of the metastatic niche, EMT, and the largely hypoxic state of the tumor microenvironment (TME). Cancer stem cells are the central drivers of metastasis due to their inherent plasticities and contribute to chemoresistance, functioning of the premetastatic niche, and induction of EMT (Sancho et al. 2016). In the premetastatic niche, extracellular signaling contributes to a TME that facilitates the development of the cancer. EMT allows cancer cells to detach from a tumor site, relocalize, and change their phenotype to a less differentiated state. When tumor growth reaches a critical point, cancerous cells deprive their environments of oxygen, resulting in hypoxia and potential metabolic shifts including the Warburg effect or oxidative phosphorylation (Sancho et al. 2016).