More information on the mechanisms underlying developmental plasticity are revealed on 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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