Barker, K. T., Houlston, R. S. (2003) Overgrowth syndromes: is dysfunctional PI3-kinase signalling a unifying mechanism? EUROPEAN JOURNAL OF HUMAN GENETICS, 11 (9). pp. 665-670. ISSN 1018-4813

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Abstract

Overgrowth syndromes: is dysfunctional PI3-kinase signalling a unifying mechanism? Studies in drosophila and animal models have shown that the phosphoinositide-3-kinase (PI3-kinase) axis plays a central role in normal development, defining the number and size of cells in tissues. Dysfunction of this pathway leads to growth anomalies and has been established to play a key role in the pathogenesis of Cowden syndrome and tuberous sclerosis. It is probable that dysfunction of this pathway is the basis of other disorders especially those typified by asymmetric overgrowth.

Item Type:	Article
Authors (ICR Faculty only):	Houlston, Richard
All Authors:	Barker, K. T., Houlston, R. S.
Uncontrolled Keywords:	overgrowth; PI3-kinase; Cowden syndrome; tuberous sclerosis; Proteus syndrome; TUMOR-SUPPRESSOR GENE; LHERMITTE-DUCLOS-DISEASE; PHOSPHOINOSITIDE 3-KINASE PATHWAY; PROTEUS-SYNDROME; CELL-SIZE; PTEN MUTATIONS; MOUSE MODEL; S6 KINASE; GERMLINE MUTATION; SOMA SIZE
Research teams:	ICR divisions > Genetics and Epidemiology > Molecular & Population Genetics ICR divisions > Molecular Pathology > Molecular & Population Genetics
Depositing User:	EPrints Services
Date Deposited:	10 Aug 2007 20:43
Last Modified:	10 Feb 2010 11:45
URI:	http://publications.icr.ac.uk/id/eprint/1439

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