Molecular and trophic mechanisms of pituitary tumourigenesis.

Abstract:

BACKGROUND:The paradox of pituitary tumours is that persistent growth is so atypical. By definition, all pituitary microadenomas regain complete trophic stability after an initial period of deregulated growth. Unlike tumours in many other organ systems, concern about significant growth of macroadenoma remnants after debulking is minimal. Despite reports of a relatively high prevalence of aneuploidy and clonal skewing in these tumours, prolonged efforts to implicate classical proto-oncogene activation and tumour suppressor mutations have been of limited success. No histological or molecular markers reliably predict behaviour. To date, the number of molecular genetic factors unequivocally linked to pituitary tumours can be counted on the fingers of one hand: (1) GNAS1 activation in acromegaly; (2) the MENIN and p27Kip1 (CDKN1B) mutations associated with multiple endocrine neoplasia type 1; (3) mutations of PRKA1RA with loss of 17q22-24 in Carney complex, and (4) aryl hydrocarbon receptor interacting protein gene mutations in 15% of familial isolated pituitary adenomas and 50% of familial isolated acromegaly. Together, these account for only a small proportion (<5%) of sporadic pituitary macroadenomas. CONCLUSION:In most instances, we still do not know what causes quantitative aberrations in trophic behaviour.

journal_name

Horm Res Paediatr

authors

Levy A

doi

10.1159/000329114

subject

Has Abstract

pub_date

2011-01-01 00:00:00

pages

2-6

eissn

1663-2818

issn

1663-2826

pii

000329114

journal_volume

76 Suppl 1

pub_type

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    pub_type: 杂志文章

    doi:10.1159/000338344

    authors: Todorova B,Salonen M,Jääskeläinen J,Tapio A,Jääskeläinen T,Palvimo J,Turpeinen U,Hämäläinen E,Räsänen M,Tenhola S,Voutilainen R

    更新日期:2012-01-01 00:00:00

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    pub_type: 临床试验,杂志文章

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    更新日期:2016-01-01 00:00:00

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    更新日期:2011-01-01 00:00:00