Cellular senescence is an important mechanism of tumor regression upon c-Myc inactivation

Proceedings of the National Academy of Sciences of the United States of America

Volumn 104, Issue 32, 2007, Pages 13028-13033

  Wu, Chi Hwa ^a   Van Riggelen, Jan ^a   Yetil, Alper ^a   Fan, Alice C ^a   Bachireddy, Pavan ^a   Felsher, Dean W ^a  

^a STANFORD UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

Oncogene addiction; Tumor maintenance; Tumorigenesis

Indexed keywords

ATM PROTEIN; ATR PROTEIN; CYCLIN DEPENDENT KINASE INHIBITOR 2A; CYCLIN DEPENDENT KINASE INHIBITOR 2B; HISTONE H3; HISTONE H4; MITOGEN ACTIVATED PROTEIN KINASE; MYC PROTEIN; PROTEIN P53;

ACETYLATION; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CELL AGING; CHROMATIN STRUCTURE; CONTROLLED STUDY; GENE INACTIVATION; HUMAN; HUMAN CELL; LIVER CELL CARCINOMA; LYMPHOMA; METHYLATION; MOUSE; NONHUMAN; ONCOGENE; OSTEOSARCOMA; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN MODIFICATION; SIGNAL TRANSDUCTION; TUMOR REGRESSION; ANIMAL; CHEMISTRY; CHROMATIN; DNA DAMAGE; NEOPLASM; ONCOGENE MYC; PATHOLOGY; PHYSIOLOGY; TUMOR SUPPRESSOR GENE;

ANIMALS; CELL AGING; CHROMATIN; DNA DAMAGE; GENES, MYC; GENES, P53; GENES, RETINOBLASTOMA; HUMANS; MAP KINASE SIGNALING SYSTEM; MICE; NEOPLASMS;

EID: 34548771087     PISSN: 00278424     EISSN: 10916490     Source Type: Journal    
DOI: 10.1073/pnas.0701953104     Document Type: Article

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