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First published online August 2, 2005


Development 132, 1606e (2005)
© The Company of Biologists Limited
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In this issue

Mature transdifferentiation: from metaplasia to neoplasia


More information on the mechanisms underlying developmental plasticity are revealed on p. 3767 by Means et al., who report that, for the exocrine pancreas, acinar-to-ductal metaplasia is achieved through the transdifferentiation of mature acinar cells. The replacement of one predominant cell type in a tissue with another – metaplasia – is often associated with an increased risk of neoplasia. But does metaplasia involve the outgrowth of a minor cell population, activation of stem cells or transdifferentiation of mature cell types? The researchers use genetic lineage labelling, molecular markers and morphological examination to track the acinar-to-ductal metaplasia induced in pancreatic epithelial explants by EGFR signalling. Their results provide compelling evidence that a latent precursor potential (plasticity) resides within mature exocrine cells. Transdifferentiation of mature mammalian cell types, the researchers conclude, may be a general mechanism for initiating metaplasia and subsequent neoplasia in epithelial tissues.


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Related articles in Development:

Pancreatic epithelial plasticity mediated by acinar cell transdifferentiation and generation of nestin-positive intermediates
Anna L. Means, Ingrid M. Meszoely, Kazufumi Suzuki, Yoshiharu Miyamoto, Anil K. Rustgi, Robert J. Coffey, Jr, Christopher V. E. Wright, Doris A. Stoffers, and Steven D. Leach
Development 2005 132: 3767-3776. [Abstract] [Full Text]  




This Article
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