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Understanding how pancreatic cancer can help diabetics

Pancreatic cancer is the fourth most frequent cause of cancer deaths. Studying metaplasia can help prevent the cell processes involved in its manifestation.


Metaplasia in the pancreatic acinar cell compartment, implicated in pancreatitis, is often a forerunner of tumour lesions and neoplasia in pancreatic cancer. Cellular metaplasia may take place when one mature cell type transdifferentiates into another. However, dedifferentiation is the first phase in the metaplasia. This kind of cellular plasticity seems to be found in adult pancreatic acinar cells. Since this loss of differentiation may turn the acinar cells into facultative stem cells, the different steps in this process and the molecular mechanisms governing it must be thoroughly investigated. The 'Acinar cell plasticity in the adult mouse pancreas' (Acinplast) project used an in vitro model of acino-ductal metaplasia to better understand the molecular mechanisms that govern this process. Research looked at which signalling pathways eventually contribute to dedifferentiation. Results indicate very early activation of Ras signalling and of its downstream MAPK and PI3K pathways. In addition, in the metaplastic process the cells take on characteristics that are similar to precursor cells and start to express stem cell markers. The project outcome will not only offer insight into acinar cell plasticity, but results will also be valuable in combating another disease. It has been shown that this cellular plasticity can be used optimally for forced transdifferentiation towards endocrine beta-cells, the cell type destroyed in diabetes (type 1). With dedifferentiation of the acinar cells, exocrine acinar and endocrine beta-cells can be guided into the endocrine lineage. This was achieved with rat acinar cells, using a conversion and interference approach. This points to the discovery of a new source of beta-cells to be used for cell replacement therapy.

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