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

Mei Ling Chen; Pei Zhang Xu; Xiao Ding Peng; William S. Chen; Grace Guzman; Ximing Yang; Antonio Di Cristofano; Pier Paolo Pandolfi; Nissim Hay

doi:10.1101/gad.1395006

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

Mei Ling Chen, Pei Zhang Xu, Xiao Ding Peng, William S. Chen, Grace Guzman, Ximing Yang, Antonio Di Cristofano, Pier Paolo Pandolfi, Nissim Hay

Research output: Contribution to journal › Article › peer-review

229 Scopus citations

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.

Original language	English (US)
Pages (from-to)	1569-1574
Number of pages	6
Journal	Genes and Development
Volume	20
Issue number	12
DOIs	https://doi.org/10.1101/gad.1395006
State	Published - Jun 15 2006
Externally published	Yes

Keywords

Cancer therapy
Endometrium carcinoma
Intestinal polyps
PIN
Thyroid and adrenal tumors

ASJC Scopus subject areas

Genetics
Developmental Biology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1101/gad.1395006

Cite this

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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.",

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AU - Chen, Mei Ling

AU - Xu, Pei Zhang

AU - Peng, Xiao Ding

AU - Chen, William S.

AU - Guzman, Grace

AU - Yang, Ximing

AU - Di Cristofano, Antonio

AU - Pandolfi, Pier Paolo

AU - Hay, Nissim

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KW - Intestinal polyps

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KW - Thyroid and adrenal tumors

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