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
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
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.