pouch. This joins a downward projection of the hypothalamus (neurohypophysis), destined to form the posterior lobe and pituitary stalk. This composite gland is distinct and separate from the primitive stomatodeum by the seventh week of gestation and further develops under the influence of the hypothalamus through a series of permissive and specific trans-acting proteins. It is fully functioning by the time of birth but retains considerable plasticity throughout life. Occasionally, cystic remnants of embryological development persist within the pituitary as Rathke's cleft cysts.
The majority of pituitary tumors are benign epithelial neoplasms that develop from adeno-hypophyseal parenchyma and, as such, resemble normal pituitary histology. In addition to the clinically relevant hormones produced by the pituitary, a number of additional pep-tides and hypothalamic hormones are known to be produced. These include, amongst many, vasoactive intestinal polypeptide, growth-hormone-releasing hormone (GHRH), somatostatin, substance P and renin. Such findings attest to the functional complexity of the gland.
In addition to the hormone-producing cells, apparently functionally inert or "null" cells are also found in the parenchyma, which also give rise to adenomas. These cells may produce either no hormone or an imperfect form with no biological activity. Multiple-hormone gene and gene receptor products are commonly seen in adenomas; for example, growth hormone (GH) gene expression occurs in 50% of prolactinomas and 30% of corticotrophic adenomas. This functional diversity may explain the occasional response of mixed somatotroph and lactotroph adenomas to dopamine receptor agonists.
The pathogenesis of pituitary adenomas is likely to be multifactorial. As with other neoplasms, the potential mechanisms of oncogene-sis fall into three groups:
• Abnormalities of genes regulating growth and development
• Abnormalities of tumor-suppressor genes
• Alterations in the genes controlling programmed cell death
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