First published online August 2, 2005
Development 132, 1606e (2005)
© The Company of Biologists Limited
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]