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Endocrine Abstracts (2016) 40 L18 | DOI: 10.1530/endoabs.40.L18

Laboratory of Neoplasia and Endocrine Differentiation P0L4, Centre for Research in Molecular Medicine and Chronic Disease (CIMUS), University Hospital Institute of Research (IDIS), University of Santiago de Compostela (USC), Santiago de Compostela, Spain.


The demonstration of postnatal stem cells in the adenopituitary (PSC) a few years ago has made us to redraw many of the cell biology concepts that we previously had for this gland. PSC organize in a three-dimensional structure, the niche, where they combine with other populations. How many populations cohabit in the niche, and which markers should we use to define cells associated to PSC we still do know not. However, we have advanced in the definition of a PSC as a cell co-expressing markers of different families of proteins: stem cell markers (e.g. Sox2, Sox9, Klf4), pituitary development factors (e.g. Prop1), epithelial markers (cytokeratins, β-catenin) and survival factors (Ret and Gfr α co-receptors and ligands). In PSC, a careful balance of expression among all these markers exists to ensure that stemness is maintained. In fact, overexpression of one marker over the others from the same family appears to indicate recruitment from the niche and loss of the stemness state. Little is known about the processes of commitment and differentiation once a stem cell has left the niche. In the other hand, once accepted that the pituitary is renewed by stem cells, we should take up in parallel the existence of physiological pathways of apoptosis for old or unfitting secretory cells. The study of how the pituitary maintains a balanced ‘cellular plasia’ will help us to better understand human disease due to insufficient (hypopituitarism) or excess (pituitary tumor) cell numbers.

Volume 40

ESE Basic Endocrinology Course on Endocrine and Neuroendocrine Cancer 2016

European Society of Endocrinology 

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