It has been an interesting problem to understand why specific hormones
are produced from specific cells. It is known that in the human anter
ior pituitary gland, tumors are classified into those of growth hormon
e (GH), prolactin (PRL), ACTH, thyroid stimulating hormone (TSH), and
gonadotrophin secreting adenomas as well as nonfunctioning adenomas. I
n human pituitary adenomas, GH secreting adenoma is usually plurihormo
nal, i.e., the adenoma not only produces GH but also PRL and TSH. TSH
secreting adenoma is also plurihormonal, and adenoma produces TSH as w
ell as GH and PRL. Thus, it was supposed that common transcriptional f
actors participate in the functional differentiation of GH, PRL, and T
SH. Pit-1 has been proposed to regulate GH, PRL, and TSH cells and the
dwarf mutants in mice were produced by Pit-1 gene mutations. Simmons
et al. (1990)observed Pit-1 protein expression in GH, PRL, and TSH cel
ls [10], in the adult rat pituitary gland although Pit-1 mRNA expressi
on was observed in all cell types (Fig. 1). Therefore it was anticipat
ed that, in human pituitary tumors, the functional expression in GH an
d TSH secreting adenomas may be under the regulation of Pit-1 protein,
We describe here the overview of transcriptional factors depicted by
immunohistochemistry and in situ hybridization.