Too much or too little: harnessing senescence to control oncogene-driven cancer.

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Too much or too little: harnessing senescence to control oncogene-driven cancer.

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2012 nî lūn-bûn

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Too much or too little: harnessing senescence to control oncogene-driven cancer.

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Too much or too little: harnessing senescence to control oncogene-driven cancer.

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Too much or too little: harnessing senescence to control oncogene-driven cancer.

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Too much or too little: harnessing senescence to control oncogene-driven cancer.

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Too much or too little: harnessing senescence to control oncogene-driven cancer.

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Too much or too little: harnessing senescence to control oncogene-driven cancer.

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P1476

Too much or too little: harnessing senescence to control oncogene-driven cancer

@en

P2093

Katherine M Hannan

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Richard B Pearson

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P2860

Hallmarks of Cancer: The Next Generation

Improved survival with vemurafenib in melanoma with BRAF V600E mutation

Effective use of PI3K and MEK inhibitors to treat mutant Kras G12D and PIK3CA H1047R murine lung cancers.

Inhibition of RNA polymerase I as a therapeutic strategy to promote cancer-specific activation of p53

AKT induces senescence in human cells via mTORC1 and p53 in the absence of DNA damage: implications for targeting mTOR during malignancy.

Cell cycle arrest is not yet senescence, which is not just cell cycle arrest: terminology for TOR-driven aging.

Mechanisms of disease: Oncogene addiction--a rationale for molecular targeting in cancer therapy.

Pro-senescence therapy for cancer treatment.

Senescence: a new weapon for cancer therapy.

An overview of the mTOR pathway as a target in cancer therapy.

P304

3147-3148

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P31

scholarly article

editorial

P356

10.4161/CC.21588

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P433

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P478

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P50

Rick Pearson

Katherine M Hannan

P577

2012-08-16T00:00:00Z

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P5875

230677805

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22894904

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3466506

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