A transformation in the mechanism by which the urokinase receptor signals provides a selection advantage for estrogen receptor-expressing breast cancer cells in the absence of estrogen

Cellular Signalling

Volumn 24, Issue 9, 2012, Pages 1847-1855

  Eastman, Boryana M ^a   Jo, Minji ^a   Webb, Drue L ^a   Takimoto, Shinako ^a   Gonias, Steven L ^a  

^a UNIVERSITY OF CALIFORNIA   (United States)

Author keywords

Breast cancer; EGF receptor; ERK; Estrogen receptor; uPAR; Urokinase type plasminogen activator

Indexed keywords

ERLOTINIB; ESTROGEN RECEPTOR; ESTROGEN RECEPTOR ALPHA; GEFITINIB; PLASMINOGEN ACTIVATOR; PROTEIN TYROSINE KINASE INHIBITOR; RAC1 PROTEIN; STEROID RECEPTOR COACTIVATOR 1; UROKINASE RECEPTOR; VASCULOTROPIN RECEPTOR; VITRONECTIN;

ANIMAL CELL; ARTICLE; BREAST CANCER; CANCER CELL; CELL CULTURE; CELL STRAIN MCF 7; CONTROLLED STUDY; ENZYME ACTIVATION; GENE AMPLIFICATION; HUMAN; HUMAN CELL; MOUSE; NONHUMAN; ONCOGENE SRC; PRIORITY JOURNAL; PROTEIN BINDING; SCID MOUSE; XENOGRAFT;

ANIMALS; BREAST NEOPLASMS; ESTROGEN RECEPTOR ALPHA; ESTROGENS; EXTRACELLULAR SIGNAL-REGULATED MAP KINASES; FEMALE; HUMANS; MICE; MICE, SCID; PROTEIN KINASE INHIBITORS; QUINAZOLINES; RECEPTORS, UROKINASE PLASMINOGEN ACTIVATOR; SIGNAL TRANSDUCTION; TUMOR CELLS, CULTURED;

EID: 84862650960     PISSN: 08986568     EISSN: 18733913     Source Type: Journal    
DOI: 10.1016/j.cellsig.2012.05.011     Document Type: Article

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