The Role of Mediators of Cell Invasiveness, Motility, and Migration in the Pathogenesis of Silent Corticotroph Adenomas
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The Role of Mediators of Cell Invasiveness, Motility, and Migration in the Pathogenesis of Silent Corticotroph Adenomas Ozgur Mete & Caroline Hayhurst & Hussein Alahmadi & Eric Monsalves & Hasan Gucer & Fred Gentili & Shereen Ezzat & Sylvia L. Asa & Gelareh Zadeh
Published online: 3 October 2013 # Springer Science+Business Media New York 2013
Abstract Silent corticotroph adenomas (SCAs) represent a distinct subset of clinically non-functioning pituitary adenomas. There are two variants of SCA; type I are densely granulated basophilic tumors and type II are sparsely granulated and chromophobic tumors. SCAs are known to be aggressive than the more common non-functioning gonadotroph adenomas (NFGAs). Cell–matrix interactions play an important role in the pathogenesis of pituitary adenomas. In this study, we compared 19 SCAs and 50 NFGAs with known fibroblast growth factor receptor-4 (FGFR4) status using semi-quantitative immunohistochemistry to localize β1-integrin, osteopontin, and O. Mete (*) : H. Gucer : S. L. Asa Department of Pathology, University Health Network, 200 Elizabeth Street, 11th floor, Toronto, ON M5G 2C4, Canada e-mail: [email protected] O. Mete : H. Gucer : S. L. Asa Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada O. Mete : F. Gentili : S. Ezzat : S. L. Asa : G. Zadeh Endocrine Oncology Site Group, Princess Margaret Hospital, Toronto, ON, Canada C. Hayhurst : H. Alahmadi : E. Monsalves : F. Gentili : G. Zadeh Department of Neurosurgery, University Health Network, Toronto, ON, Canada C. Hayhurst : H. Alahmadi : F. Gentili : G. Zadeh Department of Surgery, University of Toronto, Toronto, ON, Canada
matrix metalloproteinase-1 (MMP-1) as cytoplasmic, membranous, or mixed cytoplasmic-membranous staining to achieve scores of 1–4. Staining for β1-integrin was significantly higher in SCAs (100 %, score 3.3) than in NFGAs (96 %; score 2.6) (p =0.0482); there was no statistical difference within subgroups of SCA (type II score 3.4; type I score 2.8) (p =0.2663). Osteopontin immunoreactivity was also higher in SCAs (100 %, score 3.7) than in NFGAs (42 %, score 0.8) (p =0.0001); there was no statistical difference within subgroups of SCA (type II score 3.6; type I score 3.9) (p =0.2787). In contrast, MMP-1 immunoreactivity was lower in SCAs (89 %; score 2.5) than in NFGAs (98 %; score 3.6) (p =0.0005); there was no statistical difference within subgroups of SCA (type II score 2.7; type I score 2.0) (p = 0.30704). The MMP-1 results correlated with FGFR4 expression (NFGA 96 %, type II SCA 71 %, type I SCA 40 %). Our data indicate that the biological aggressivity of SCAs compared with NFGA may be due to high osteopontin expression; in contrast, high MMP-1 is characteristic of NFGAs that also express more FGFR4. Further investigations are warranted to clarify the underlying regulatory mechanisms of these markers. The high osteopontin or FGFR4/MMP-1 expression levels in SCAs and NFGAs, respectively, indicate the potential for therapeutic strategies targeting osteoponti
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