Author/Editor		Clayton, RN; Farrell, WE
Title		Molecular pathogenesis of human pituitary tumours
Type		članek
Source		In: Mrevlje F, editor. SEK. Zbornik povzetkov predavanj in posterskih predstavitev 1. slovenski endokrinološki kongres z mednarodno udeležbo; 1998 okt 1-3; Radenci. Ljubljana: Združenje endokrinologov Slovenije,
Publication year		1998
Volume		str. 12-6
Language		eng
Abstract		The purpose of this review is to highlight recent studies that have advanced our understanding of the underlying mechanisms responsible for both pituitary tumour initation and progression, thereby possibly proving reliable prognostic markers of tumour behaviour. The paradigm for tumour initiation and progression is perhaps best exemplified in corolectar cancer. In these tumours the sequential histological changes from hyperplasia through to carcinoma have been described, together with the progressive accumulation of genetic aberrations in both oncogenes and tumour suppressor genes (TSG's). Although a similar multi-step aetiology involving both oncogenes and TSG's has been proposed for the development of endocrine tumours many of the changes are less well defined owing, in part , to the rarity of the invasive and malignant phenotype. X-chromosal inactivation analysis in tumours from female patients has confirmed a monoclonal origin in the majority. Although these data strongly support the view that pituitary adenomas result from a clonal expansion of a single mutated pituitary ceel the importance of facilitatory hypothalamic factors and peripheral hormones controlling tumour progression are highlighted by clinical findings and have been recently reviewed (Herman and Fagin 1995, Shimon and Melmed 1997). Progression through the cell cycle is normally tightly regulated, involving a cascade of genes and their protein products that signal a cell to divide (proto-ancogenes) or remain quiescent (TSG's). Aberrations in these pathways, leading to a selective growth advantage, are a hallmark of tumorigenesis. Oncogenes are responsible for a gain of function, whilst the TSG's are tumorigenic through a loss of function.
Descriptors		PITUITARY NEOPLASMS GENES, SUPPRESSOR, TUMOR ALLELES GENES, RETINOBLASTOMA