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The Role of Hormones, Growth Factors and Their Receptors in Pituitary Tumorigenesis
Author(s) -
Ezzat Shereen
Publication year - 2001
Publication title -
brain pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.986
H-Index - 132
eISSN - 1750-3639
pISSN - 1015-6305
DOI - 10.1111/j.1750-3639.2001.tb00405.x
Subject(s) - endocrinology , medicine , biology , pituitary tumors , hormone , receptor , acromegaly , hyperplasia , adenoma , prolactin cell , hypothalamic hormones , carcinogenesis , prolactin , pituitary adenoma , pars tuberalis , pituitary gland , cancer research , cancer , pituitary hormones , growth hormone
Numerous factors have been shown to govern adenohypophysial cell proliferation. Human and animal models have documented that the hypothalamic trophic hormone growth hormone‐releasing hormone stimulates cell proliferation, and prolonged stimulation leads to tumor formation. Similarly, lack of dopaminergic inhibition of lactotrophs and lack of feedback suppression by adrenal, gonadal or thyroid hormones are implicated, perhaps through hypothalamic stimulatory mechanisms, in pituitary adenoma formation superimposed on hyperplasia. However, most pituitary tumors are not associated with underlying hyperplasia. Overexpression of growth factors and their receptors, such as EGF, TGFα, EGF‐R and VEGF has been identified in pituitary adenomas, and reduction of follistatin expression has been implicated in gonadotroph adenomas. Aberrant expression of members of the FGF family, an FGF antisense gene and FGF receptors have all been described in pituitary adenomas. The clonal composition of pituitary adenomas attests to the molecular basis of pituitary tumorigenesis, however, the evidence suggests that these various hypophysiotropic hormones and growth factors likely play a role as promoters of tumor cell growth in genetically transformed cells.

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