PTEN deficiency is fully penetrant for prostate adenocarcinoma in C57BL/6 mice via mTOR-dependent growth.
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Therapeutic targeting of cancers with loss of PTEN function.mTOR signaling in tumorigenesisBiochemical and cellular evidence demonstrating AKT-1 as a binding partner for resveratrol targeting protein NQO2Targeting ASCT2-mediated glutamine uptake blocks prostate cancer growth and tumour developmentThe effects of aging on the molecular and cellular composition of the prostate microenvironment.Rapamycin is a potent inhibitor of skin tumor promotion by 12-O-tetradecanoylphorbol-13-acetate.Cooperation between Stat3 and Akt signaling leads to prostate tumor development in transgenic mice.Slow disease progression in a C57BL/6 pten-deficient mouse model of prostate cancer.Rapamycin and mTORC1 inhibition in the mouse: skin cancer prevention.Animal models relevant to human prostate carcinogenesis underlining the critical implication of prostatic stem/progenitor cells.Loss of ATF3 promotes Akt activation and prostate cancer development in a Pten knockout mouse modelPten regulates collective cell migration during specification of the anterior-posterior axis of the mouse embryo.Obesity, energy balance, and cancer: new opportunities for preventionApigenin inhibits prostate cancer progression in TRAMP mice via targeting PI3K/Akt/FoxO pathwayPTEN loss in the continuum of common cancers, rare syndromes and mouse models.Targeting the PI3K signaling pathway in cancer therapy.Leading causes of castration-resistant prostate cancer.LAT1 is a putative therapeutic target in endometrioid endometrial carcinoma.In vivo quantitative phosphoproteomic profiling identifies novel regulators of castration-resistant prostate cancer growth.Crosstalk of the EphA2 receptor with a serine/threonine phosphatase suppresses the Akt-mTORC1 pathway in cancer cells.Effect of Metformin, Rapamycin, and Their Combination on Growth and Progression of Prostate Tumors in HiMyc Mice.Timp3 loss accelerates tumour invasion and increases prostate inflammation in a mouse model of prostate cancer.INPP4B is highly expressed in prostate intermediate cells and its loss of expression in prostate carcinoma predicts for recurrence and poor long term survival.Dietary energy balance modulation of epithelial carcinogenesis: a role for IGF-1 receptor signaling and crosstalk.
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P2860
PTEN deficiency is fully penetrant for prostate adenocarcinoma in C57BL/6 mice via mTOR-dependent growth.
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article científic
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article scientifique
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articolo scientifico
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artigo científico
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bilimsel makale
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scientific article published on May 2009
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
PTEN deficiency is fully penet ...... ice via mTOR-dependent growth.
@en
PTEN deficiency is fully penet ...... ice via mTOR-dependent growth.
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type
label
PTEN deficiency is fully penet ...... ice via mTOR-dependent growth.
@en
PTEN deficiency is fully penet ...... ice via mTOR-dependent growth.
@nl
prefLabel
PTEN deficiency is fully penet ...... ice via mTOR-dependent growth.
@en
PTEN deficiency is fully penet ...... ice via mTOR-dependent growth.
@nl
P2093
P2860
P1476
PTEN deficiency is fully penet ...... ice via mTOR-dependent growth.
@en
P2093
Angela Alexander
Bhuvanesh Dave
Cheryl Lyn Walker
Claudio J Conti
Fernando Benavides
Gordon Mills
Jorge Blando
Melisa Portis
P2860
P304
P356
10.2353/AJPATH.2009.080055
P407
P577
2009-05-01T00:00:00Z