From prolactin cell to prolactinoma
Velkeniers, B.
Verhandelingen - Koninklijke Academie Voor Geneeskunde van Belgie 63(6) 561-573; Discussion: 574-576
2001
ISSN/ISBN: 0302-6469 PMID: 11813510 Document Number: 533964
The pathogenesis, diagnosis and treatment of common pituitary neoplasms is based on the understanding of the differentiated hormone expression by specific pituitary cell types and of the central hypothalamic, peripheral and local control of their hormonal secretion (endocrine, autocrine, paracrine regulation). Tumorigenesis is the result of a complex multistep process. It is likely that a molecular genetic alteration initially leads to cell transformation. Nevertheless the transformed cell is dependent on hormonal and/or growth factor stimulation for tumor progression. This cascade is responsible for autonomic hormone secretion, and cell proliferation. PRL cells do not behave identically in terms of cell function. Functional diversity among PRL cells is documented in vitro, in terms of basal and synthetic capacity and in respect to responsiveness to dopamine and oestrogen regulation. These in vitro observations can be extended to the in vivo situation. In the intact pituitary, PRL cells differ in their relative content of PRL and their response to secretagogues. These differences relate to their topographical localization within the pituitary. Prolactinoma are mainly composed of cells with a high basal synthetic and secretory capacity and arise preferentially in the peripheral parts of the hypophysis. It is therefore tempting to postulate that the "in situ milieu" within the pituitary is relevant for the development of prolactinoma. By stimulating growth in certain areas, there is an increased probability of mutation. At the same time growth of a mutated PRL cell could be stimulated.