Ink4a/Arf loss promotes tumor recurrence following Ras inhibition

Neuro-Oncology

Volumn 14, Issue 1, 2012, Pages 34-42

  Van Brocklin, Matthew W ^a   Robinson, James P ^a   Lastwika, Kristin J ^a   McKinney, Andrea J ^a   Gach, H Michael ^a   Holmen, Sheri L ^a,b  

^a NEVADA CANCER INSTITUTE   (United States)

^b UNIVERSITY OF UTAH   (United States)

Author keywords

Glioma; Ink4a Arf; Mouse; Ras; Tumor maintenance

Indexed keywords

CYCLIN DEPENDENT KINASE INHIBITOR 2A; DOXYCYCLINE; MITOGEN ACTIVATED PROTEIN KINASE; PROTEIN KINASE B;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; CANCER RECURRENCE; CANCER STAGING; CANCER SURGERY; CONTROLLED STUDY; DISEASE MODEL; DOWN REGULATION; ENZYME REACTIVATION; GENE EXPRESSION; GLIOBLASTOMA; GLIOMA; IN VIVO STUDY; MOUSE; NONHUMAN; ONCOGENE K RAS; PROTEIN DEPLETION; SIGNAL TRANSDUCTION; TUMOR GROWTH; TUMOR RECURRENCE; TUMOR REGRESSION;

ANIMALS; BRAIN NEOPLASMS; CELL LINE, TUMOR; CYCLIN-DEPENDENT KINASE INHIBITOR P16; DISEASE MODELS, ANIMAL; GENE EXPRESSION REGULATION, NEOPLASTIC; GENES, P16; GENETIC VECTORS; GLIOMA; HUMANS; MICE; MICE, TRANSGENIC; MITOGEN-ACTIVATED PROTEIN KINASES; NEOPLASM RECURRENCE, LOCAL; ONCOGENIC VIRUSES; PROTO-ONCOGENE PROTEINS P21(RAS); SIGNAL TRANSDUCTION;

EID: 84856259077     PISSN: 15228517     EISSN: 15235866     Source Type: Journal    
DOI: 10.1093/neuonc/nor184     Document Type: Article

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