GS-ALPHA, PROTEIN-KINASE-C, CATHEPSIN-D, GROWTH-FACTORS, ESTROGEN RECEPTOR-RELATED PROTEIN, AND P53 IN PROLACTIN CELL ADENOMAS AND NULL-CELL ADENOMAS OF THE PITUITARY

Citation
L. Wellhausen et al., GS-ALPHA, PROTEIN-KINASE-C, CATHEPSIN-D, GROWTH-FACTORS, ESTROGEN RECEPTOR-RELATED PROTEIN, AND P53 IN PROLACTIN CELL ADENOMAS AND NULL-CELL ADENOMAS OF THE PITUITARY, Endocrine pathology, 9(2), 1998, pp. 135-148
Citations number
50
Categorie Soggetti
Pathology,"Endocrynology & Metabolism
Journal title
ISSN journal
10463976
Volume
9
Issue
2
Year of publication
1998
Pages
135 - 148
Database
ISI
SICI code
1046-3976(1998)9:2<135:GPCGER>2.0.ZU;2-5
Abstract
The aim of the present study was to assess the prevalence of the expre ssion pattern of different growth factors and growth-related signaling and transport proteins, including the a-subunit of stimulatory G-prot ein, protein kinase C (PKC), cathepsin D, epidermal growth factor (EGF ), transforming growth factor-alpha (TGF-alpha), insulin-like growth f actor-1 (IGF-1), estrogen receptor-related protein (p29), and p53 in h uman pituitary tumors. Immunohistochemistry (IHC) was performed by scr eening tissue sections from 32 patients, including 18 prolactin cell a denomas and 14 null cell adenomas. IHC demonstrated an increased react ivity for Gs alpha in 6 prolactin cell and 12 null cell adenomas. PKC had a weak immunoreactivity in all pituitary adenomas. Cathepsin D was absent in the majority of pituitary adenomas. The remaining adenomas showed weak positivity in some scattered tumor cells. Low levels of EG F expression were found in 13 prolactin cell and 3 null cell adenomas. Immunoreactivity for TGF-alpha and IGF-1 was observed in all cases. T he prolactin cell adenomas exhibited stronger TGF-alpha- and IGF-1 lab eling compared with the null cell adenomas. The estrogen receptor-rela ted protein (p29) was identified in only one prolactin cell adenoma. p 53 protein expression was not present in any pituitary sample. It is s uggested that Gs alpha overexpression, PKC, growth factors, and absent or decreased p29 expression may be involved in pituitary tumorigenesi s. p53 and cathepsin D appear to play no consistent role in the pathog enesis of pituitary adenomas.