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SRP (Groeiers): Regenerative therapy in diabetes (SRP35)

Diabetes results from an insufficient number of insulin-secreting beta cells in the pancreas. In the case of Type 1 diabetes there is a gradual depletion of the beta cell mass whereas in Type 2 diabetes the beta cells fail to increase their number to compensate for increased insulin demands. Transplantation of beta cells from cadaveric organ donors has the potential to cure T1D but this therapy is significantly hampered by the shortage of organ donors.

Our long term mission is to contribute to the search for alternative sources of beta cells for replacement therapy, and to find new ways for regeneration of a functional beta cell mass within the pancreas.

To reach this aim we envision to elaborate the following significant specific aims to which our research teams already made major breakthrough contributions: (i) differentiation of adult facultative pancreatic stem/progenitor cells, (ii) proliferation of newly-formed and pre-existing beta cells, (iii) transdifferentiation of exocrine acinar to endocrine beta cells, and (iv) differentiation of pluripotent (embryonic) stem cells.
Date:1 Mar 2014 →  28 Feb 2019
Keywords:Immunocytochemistry, Endocrine Pancreatic Tumors, Apoptosis, Development, Zollinger Ellison Syndrome, Cancer, Diabetes, Cell Biology, Histology, Morphogenesis Of Endocrine Pancreas, Microscopy, Morphology, Cell Growth And Differentiation, Men-I, Islet Cell Transplantation, pancreas, endocrine
Disciplines:Cancer therapy