Steroid hormone receptor in pleural solitary fibrous tumours and CD34+ progenitor stromal cells
- PMID: 12237886
- DOI: 10.1002/path.1195
Steroid hormone receptor in pleural solitary fibrous tumours and CD34+ progenitor stromal cells
Abstract
Solitary fibrous tumours (SFT), originally described in the pleura, were subsequently recognized in numerous extrapleural sites. This suggests that a common stem cell, present in various organs and tissues, may be at the origin of SFT and that specific factors may be involved in the proliferation of such cells. Recently it has been described that steroid hormone receptors, progesterone receptors in particular, are expressed by extrapleural SFT. In addition, progesterone may participate as growth factor in many CD34(+) stromal neoplasms, which express low levels of the hormone receptors. The present study analysed the expression of androgen (AR), oestrogen (ER) and progesterone (PR) receptors in a series of 32 pleural SFT, 10 mesotheliomas and in reactive tissue of chronic pleuritis. ER and AR were never expressed by SFT or by chronic pleuritis, whereas PR were demonstrated in 2/16 "large" (>8 cm) and in 6/16 "small" (< or =8 cm) pleural SFT (all expressing CD34, bcl-2 and CD99). PR(+) SFT had a significantly higher proliferative activity (p = 0.04) (Ki-67 mean value 6.5%) and lower p27(kip1) (mean value 51.5%) expression than the PR(-) cases (Ki-67 mean value 3.81% and p27(kip1) mean value 57.86%). One of the cases expressing a high level of PR (80%) recurred 1 year after first surgery and the recurrence was PR(+) as well, but with a lower percentage of nuclear receptor expression (12%). In addition, in chronically inflamed subserosal tissue, a subpopulation of CD34(+) endothelial and interstitial dendritic cells was identified, which also expressed PR. These findings suggest that the CD34(+) submesothelial interstitial dendritic cells, activated during reactive processes, may be the stem cells that give rise to SFT, and that progesterone might participate in the growth of SFT through modulation of its specific receptors.
Copyright 2002 John Wiley & Sons, Ltd.
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