EXPRESSION OF THE TRANSFERRIN RECEPTOR IN HUMAN ANTERIOR-PITUITARY ADENOMAS IS CONFINED TO GONADOTROPHINOMAS

Citation
Sl. Atkin et al., EXPRESSION OF THE TRANSFERRIN RECEPTOR IN HUMAN ANTERIOR-PITUITARY ADENOMAS IS CONFINED TO GONADOTROPHINOMAS, Clinical endocrinology, 44(4), 1996, pp. 467-471
Citations number
26
Categorie Soggetti
Endocrynology & Metabolism
Journal title
ISSN journal
03000664
Volume
44
Issue
4
Year of publication
1996
Pages
467 - 471
Database
ISI
SICI code
0300-0664(1996)44:4<467:EOTTRI>2.0.ZU;2-B
Abstract
OBJECTIVE The human pituitary gland is affected selectively by conditi ons associated with iron deposition, but the mechanisms for this are u nknown. In this study we have determined whether the transferrin recep tor, which mediates iron uptake by cells, could be detected immunocyto chemically in human pituitary adenomas in vitro. PATIENTS Data were de rived from 35 patients undergoing transsphenoidal surgery and included 13 with clinically non-functioning adenomas, 15 with acromegaly, 4 pr olactinomas, 2 patients with Gushing's disease and one patient with Ne lson's syndrome. MEASUREMENTS Transferrin receptor immunopositivity wa s determined for each adenoma in dispersed cell culture using a specif ic monoclonal antibody. RESULTS Eight of 13 clinically functionless ad enomas showed immunopositive transferrin receptor expression, whilst a denomas from 15 patients with acromegaly, 4 prolactinomas, 2 Cushing's syndrome and one patient with Nelson's syndrome were negative. The ei ght transferrin receptor positive tumours were gonadotrophinomas and a ccounted for eight of the nine tumours which secreted and immunostaine d for FSH; all eight also secreted and immunostained for LH. CONCLUSIO NS These findings may reflect a special requirement for iron by gonado trophin secreting cells in comparison to other pituitary cell types an d this could underlie the reasons why in the normal pituitary these ce lls are especially susceptible to malfunction in iron overload syndrom es such as genetic haemochromatosis and beta-thalassaemia.