The deficiency of Akt1 is sufficient to suppress tumor development in Pten+/- mice Journal Article

   

Authors:	Chen, M. L.; Xu, P. Z.; Peng, X. D.; Chen, W. S.; Guzman, G.; Yang, X.; Di Cristofano, A.; Pandolfi, P. P.; Hay, N.
Article Title:	The deficiency of Akt1 is sufficient to suppress tumor development in Pten+/- mice
Abstract:	The tumor suppressor PTEN is frequently inactivated in human cancers. A major downstream effector of PTEN is Akt, which is hyperactivated via PTEN inactivation. It is not known, however, whether diminished Akt activity is sufficient to inhibit tumorigenesis initiated by Pten deficiency. Here we showed that the deficiency of Akt1 is sufficient to dramatically inhibit tumor development in Pten+/- mice. Akt1 deficiency had a profound effect on endometrium and prostate neoplasia, two types of human cancer, in which PTEN is frequently mutated, and also affected thyroid and adrenal medulla tumors and intestinal polyps. Even haplodeficiency of Akt1 was sufficient to markedly attenuate the development of highgrade prostate intraepithelial neoplasia (PIN) and endometrial carcinoma. These results have significant implications for cancer therapy. © 2006 by Cold Spring Harbor Laboratory Press.
Keywords:	protein kinase b; controlled study; nonhuman; endometrium carcinoma; endometrial neoplasms; neoplasms; animal cell; mouse; animals; mice; animal tissue; animal experiment; animal model; heterozygote; cancer therapy; carcinogenesis; haplotype; prostate cancer; prostatic neoplasms; cancer inhibition; phosphatidylinositol 3,4,5 trisphosphate 3 phosphatase; proto-oncogene proteins c-akt; pten phosphohydrolase; thyroid neoplasms; prostatic intraepithelial neoplasia; thyroid tumor; adrenal gland neoplasms; endometrium; enzyme deficiency; intestine polyp; pseudolymphoma; intestinal polyps; pin; thyroid and adrenal tumors; adrenal medulla tumor
Journal Title:	Genes and Development
Volume:	20
Issue:	12
ISSN:	0890-9369
Publisher:	Cold Spring Harbor Laboratory Press
Date Published:	2006-06-15
Start Page:	1569
End Page:	1574
Language:	English
DOI:	10.1101/gad.1395006
PUBMED:	16778075
PROVIDER:	scopus
PMCID:	PMC1482477
DOI/URL:	http://www.scopus.com/inward/record.url?eid=2-s2.0-33745172528&partnerID=40&md5=27577ced5f69bcfee8bb55bc217a9021
Notes:	--- - "Cited By (since 1996): 114" - "Export Date: 4 June 2012" - "CODEN: GEDEE" - "Source: Scopus"

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