Transformation by HrasG12V is consistently associated with mutant allele copy gains and is reversed by farnesyl transferase inhibition

Oncogene

Volumn 33, Issue 47, 2013, Pages 5442-5449

  Chen, X ^a   Makarewicz, J M ^a   Knauf, J A ^a   Johnson, L K ^a   Fagin, J A ^a,b  

^a MEMORIAL SLOAN KETTERING CANCER CENTER   (United States)

^b WEILL CORNELL MEDICAL COLLEGE   (United States)

Author keywords

Farnesyl transferase inhibitor; Papilloma; RAS

Indexed keywords

7,12 DIMETHYLBENZ[A]ANTHRACENE; DIMETHYLBENZ[A]ANTHRACENE; KI 67 ANTIGEN; LONAFARNIB; MAMMALIAN TARGET OF RAPAMYCIN; MESSENGER RNA; MITOGEN ACTIVATED PROTEIN KINASE; MITOGEN ACTIVATED PROTEIN KINASE 1; NICOTINAMIDE ADENINE DINUCLEOTIDE ADENOSINE DIPHOSPHATE RIBOSYLTRANSFERASE; PHORBOL 13 ACETATE 12 MYRISTATE; PROTEIN FARNESYLTRANSFERASE; PROTEIN FARNESYLTRANSFERASE INHIBITOR; PROTEIN KINASE B;

ALLELE; ALLELIC IMBALANCE; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CANCER GROWTH; CANCER INHIBITION; CONTROLLED STUDY; DRUG EFFICACY; ENZYME INHIBITION; FARNESYLATION; GENE DOSAGE; HUMAN; HUMAN CELL; IN VITRO STUDY; LASER CAPTURE MICRODISSECTION; MOUSE; NONHUMAN; ONCOGENE H RAS; ONCOGENE K RAS; ONCOGENE N RAS; PRIORITY JOURNAL; PROTEIN LOCALIZATION; SKIN CARCINOGENESIS; SKIN PAPILLOMA;

EID: 84887521253     PISSN: 09509232     EISSN: 14765594     Source Type: Journal    
DOI: 10.1038/onc.2013.489     Document Type: Article

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