ArticleThe American journal of pathology2009
PTEN deficiency is fully penetrant for prostate adenocarcinoma in C57BL/6 mice via mTOR-dependent growth.
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 44 citations in OpenAlex.
- Review
- Review
- DEPTOR is an in vivo tumor suppressor that inhibits prostate tumorigenesis via the inactivation of mTORC1/2 signals.Oncogene · 2020Article
- Loss of ATF3 promotes Akt activation and prostate cancer development in a Pten knockout mouse model.Oncogene · 2015Article
- Effect of Metformin, Rapamycin, and Their Combination on Growth and Progression of Prostate Tumors in HiMyc Mice.Cancer prevention research (Philadelphia, Pa.) · 2015Article
- Targeting ASCT2-mediated glutamine uptake blocks prostate cancer growth and tumour development.The Journal of pathology · 2015Article
- In vivo quantitative phosphoproteomic profiling identifies novel regulators of castration-resistant prostate cancer growth.Oncogene · 2015Article
- mTOR signaling in tumorigenesis.Biochimica et biophysica acta · 2014Review
- Apigenin inhibits prostate cancer progression in TRAMP mice via targeting PI3K/Akt/FoxO pathway.Carcinogenesis · 2014Article
- Therapeutic targeting of cancers with loss of PTEN function.Current drug targets · 2014Article
- Biochemical and cellular evidence demonstrating AKT-1 as a binding partner for resveratrol targeting protein NQO2.PloS one · 2014Article
- Obesity, energy balance, and cancer: new opportunities for prevention.Cancer prevention research (Philadelphia, Pa.) · 2012Review
- Pten regulates collective cell migration during specification of the anterior-posterior axis of the mouse embryo.Developmental biology · 2012Article
- Animal models relevant to human prostate carcinogenesis underlining the critical implication of prostatic stem/progenitor cells.Biochimica et biophysica acta · 2011Review
- Rapamycin and mTORC1 inhibition in the mouse: skin cancer prevention.Cancer prevention research (Philadelphia, Pa.) · 2011Article
- Rapamycin is a potent inhibitor of skin tumor promotion by 12-O-tetradecanoylphorbol-13-acetate.Cancer prevention research (Philadelphia, Pa.) · 2011Article
- Slow disease progression in a C57BL/6 pten-deficient mouse model of prostate cancer.The American journal of pathology · 2011Article
- PTEN loss in the continuum of common cancers, rare syndromes and mouse models.Nature reviews. Cancer · 2011Review
- Cooperation between Stat3 and Akt signaling leads to prostate tumor development in transgenic mice.Neoplasia (New York, N.Y.) · 2011Article
- Crosstalk of the EphA2 receptor with a serine/threonine phosphatase suppresses the Akt-mTORC1 pathway in cancer cells.Cellular signalling · 2011Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 3 countries.
Funding
Abstract
The tumor suppressor phosphatase and tensin homolog (PTEN) is frequently involved in human prostate carcinoma. PTEN is therefore an attractive target for the development of preclinical animal models. Prostate intraepithelial neoplasia lesions develop in mice with Pten heterozygosity, but disease progression has been reported only in combination with either other tumor suppressor gene alterations or the conditional inactivation of both Pten alleles in prostate epithelial cells. We report that on a C57BL/6 background, in contrast to previous studies on mixed 129 genetic backgrounds, Pten locus heterozygosity is fully penetrant for the development of prostate adenocarcinoma. Grossly observable tumors were detected at 6 months of age, and, by 10 to 12 months, 100% of examined mice developed adenocarcinoma of the anterior prostate. Furthermore, double heterozygotes carrying both Pten and Tsc2-null alleles showed no increase relative to Pten(+/-) heterozygotes in either lesion development or progression. Lesions in both Pten(+/-); Tsc2(+/-), and Pten(+/-) mice exhibited loss of PTEN expression and activation of PI3K signaling. PI3K activation occurred early in prostate intraepithelial neoplasia lesion formation in these animals, consistent with loss of PTEN function, and contributed to the etiology of tumors that developed in Pten(+/-) mice. Furthermore, prostate lesion growth in Pten(+/-) mice was dependent on mTOR, as evidenced by a reduction in both phospho-S6 levels and proliferative index after rapamycin treatment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.