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*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

228 Scopus citations


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 languageEnglish (US)
Pages (from-to)1569-1574
Number of pages6
JournalGenes and Development
Issue number12
StatePublished - Jun 15 2006


  • Cancer therapy
  • Endometrium carcinoma
  • Intestinal polyps
  • PIN
  • Thyroid and adrenal tumors

ASJC Scopus subject areas

  • Genetics
  • Developmental Biology


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