Defects in transforming growth factor-β signaling cooperate with a Ras oncogene to cause rapid aneuploidy and malignant transformation of mouse keratinocytes

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

Volumn 96, Issue 26, 1999, Pages 14949-14954

  Glick, Adam ^a   Popescu, Nicholas ^a   Alexander, Valarie ^a   Ueno, Hikaru ^b   Bottinger, Erwin ^c   Yuspa, Stuart H ^a  

^a NATIONAL CANCER INSTITUTE   (United States)

^b KYUSHU UNIVERSITY   (Japan)

^c ALBERT EINSTEIN COLLEGE OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

TRANSFORMING GROWTH FACTOR BETA;

ANEUPLOIDY; ANIMAL CELL; ARTICLE; CHROMOSOME ABERRATION; CHROMOSOME BREAKAGE; GENE EXPRESSION; GENE INACTIVATION; GENE REPRESSION; GENETIC TRANSDUCTION; KERATINOCYTE; MALIGNANT TRANSFORMATION; MOUSE; NEWBORN; NONHUMAN; ONCOGENE RAS; PRIORITY JOURNAL; PROTEIN DEFECT; SIGNAL TRANSDUCTION; SQUAMOUS CELL CARCINOMA; TUMOR GROWTH;

ANEUPLOIDY; ANIMALS; CALCIUM; CARCINOMA, SQUAMOUS CELL; CELL TRANSFORMATION, NEOPLASTIC; DOSE-RESPONSE RELATIONSHIP, DRUG; DRUG RESISTANCE; GENES, RAS; KERATINOCYTES; MICE; MICE, MUTANT STRAINS; RECEPTORS, TRANSFORMING GROWTH FACTOR BETA; SIGNAL TRANSDUCTION; TRANSDUCTION, GENETIC; TRANSFORMING GROWTH FACTOR BETA;

ADENOVIRIDAE; ANIMALIA;

EID: 0033593025     PISSN: 00278424     EISSN: None     Source Type: Journal    
DOI: 10.1073/pnas.96.26.14949     Document Type: Article

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