The p53 inducing drug dosage may determine quiescence or senescence

Aging

Volumn 2, Issue 11, 2010, Pages 748-

  Lane, David P ^a   Verma, Chandra ^a   Fang, Cheok Chit ^a  

^a AGENCY FOR SCIENCE   (Singapore)

Author keywords

[No Author keywords available]

Indexed keywords

IMIDAZOLE DERIVATIVE; MAMMALIAN TARGET OF RAPAMYCIN; NUTLIN 3; PIPERAZINE DERIVATIVE; PROTEIN P53;

ANIMAL; ARTICLE; BREAST TUMOR; CELL AGING; CELL CYCLE; FEMALE; GENETICS; HUMAN; METABOLISM; PHYSIOLOGY;

ANIMALS; BREAST NEOPLASMS; CELL AGING; CELL CYCLE; FEMALE; HUMANS; IMIDAZOLES; PIPERAZINES; TOR SERINE-THREONINE KINASES; TUMOR SUPPRESSOR PROTEIN P53;

EID: 79952691843     PISSN: 19454589     EISSN: None     Source Type: Journal    
DOI: 10.18632/aging.100229     Document Type: Note

References (8)

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3. Huang B et al. Pharmacologic p53 activation blocks cell cycle progression but fails to induce senescence in epithelial cancer cells. Mol Cancer Res. 2009; 7:1497-3509.
4. Ventura A et al. Restoration of p53 function leads to tumour regression in vivo. Nature. 2007; 445:661-665.
5. Xue W et al. Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas. Nature. 2007; 445:656-660.
6. Leontieva OV et al. Weak p53 permits senescence during cell cycle arrest. Cell Cycle. 2010; 9: 4323-4327.
7. Bertheau P et al. Exquisite sensitivity of TP53 mutant and basal breast cancers to a dose-dense epirubicin-cyclophosphamide regimen. PLoS Med. 2007; 4:e90.
8. Varna M et al. Int J Cancer. 2009; 124:991-997.