Immunohistochemical analysis of major @entity2533 isoforms and their receptors in XXXX .

@entity1 @entity5 @entity3985 @entity957 @entity189 @entity2533
We analyzed immunohistochemically the tissue distribution of the three major transforming growth factors-beta isoforms ( @entity2533 ) in tissue samples from 38 @entity1 with @entity957 . Besides a qualitative evaluation, the number of the respectively labeled cells was determined by morphometric analysis. In all @entity5 samples a significant staining of most @entity5 cells was seen both for the @entity2533 isoforms and the TBRs. Similarly, the majority of stromal cells were labeled. On semiserial sections, there were only minor differences in the distribution pattern and in the number of labeled cells between the three @entity2533 isoforms and the TBRs, suggesting that most @entity5 cells are actively involved in the neosynthesis of TGF-betas and TBRs; accordingly, at least most @entity5 cells seem to be capable of producing more than one @entity2533 form and in parallel several TBRs. With decreasing @entity5 cell differentiation the number of @entity2533 - and TBR-positive @entity5 cells decreased slightly (but not to a statistically significant degree). Interestingly, the stromal cells were labeled for TGF-betas and TBRs to a lower extent than the epithelial cells, and there was no significant difference between non- @entity5 -associated control stroma and the immediate peritumoral stroma. Our observations suggest an even, enhanced level of @entity2533 production in @entity957 , which may explain some well-known side-effects of @entity5 growth, such as @entity3985 . In addition, the presence of immunoreactive TBR-proteins in the vast majority of @entity5 cells excludes the mere absence of TBRs in those @entity189 as the cause for inappropriate @entity2533 function in the @entity5 cells. This in turn suggests that molecular alterations either of the TBR-proteins non-affecting the synthesis and turnover or downstream alterations of the @entity2533 signaling pathway may be main reasons for the loss of response of the @entity5 cells to the enhanced amounts of TGF-betas.
