title: Stem cells might participate in the cell turnover of duodenal adenomas.
abstract: Eighty-three duodenal adenomas were stained with hematoxylin-eosin (H&E) and with anti-lysozyme immunostain. Mature Paneth cells were those showing coarse brightly red cytoplasmic granules in H&E stain and Paneth cell precursors were those lysozyme-expressing cells that had remained undetected in H&E stain. In the adenomas, the number of mature Paneth cells/high power field varied from 4 to 12 (mean 6.5) in H&E stain, and of lysozyme-expressing cells from 32 to 62 (mean 46.5) (p<0.05). Lysozyme-expressing cells were found haphazardly distributed within the histological profile of the lesion, even in the most superficial cell layer of the dysplastic glands. The latter suggests that if the innate programmed vector of cell migration were valid for duodenal adenomas (from stem cells towards the bottom of the crypts for Paneth cells) the stem cells, normally overlaying Paneth cells, would have been exfoliated into the lumen. Another, less likely option, is that mutated stem cells at the bottom of duodenal adenomas translocate, in an unprecedented manner, the ontogenic signals of migration for Paneth cells. This stochastic molecular option would imply a total reversal of the normal migratory vector for Paneth cells, to a more aberrant, paradoxical migration flow, from stem cells to the villus domain, before exfoliation. Because of the unique migratory direction of the Paneth cells in the crypts of Lieberkühn, the duodenal adenoma emerges as a suitable histo-biological model to monitor the fate of stem cells. It is suggested that stem cells, together with the other recordable mature cells, namely dysplastic enterocytes, Paneth cells and goblet cells, participate in the cell turnover of duodenal adenomas. Further studies are necessary to definitively validate the abovementioned suggested hypothesis.
authors.affiliation: Gastrointestinal and Liver Pathology Research Laboratory, Department of Pathology, Karolinska Institute and University Hospital 17176, Stockholm, Sweden. Carlos.Rubio@onkpat.ki.se
authors.forename: Carlos A
authors.initials: CA
authors.lastname: Rubio