Amplification of the driving oncogene, KRAS or BRAF, underpins acquired resistance to MEK1/2 inhibitors in colorectal cancer cells (Science Signaling (2011) 4 (er2))

Science Signaling

Volumn 4, Issue 170, 2011, Pages

  Little, A S ^a   Balmanno, K ^a   Sale, M J ^a   Newman, S ^a   Dry, J R ^a   Hampson, M ^a   Edwards, P A W ^a   Smith, P D ^a   Cook, S J ^a  

^a NONE

Author keywords

[No Author keywords available]

Indexed keywords

ERRATUM; ERROR; PRIORITY JOURNAL; ARTICLE; CELL CYCLE; CELL DEATH; COLORECTAL TUMOR; DRUG ANTAGONISM; DRUG EFFECT; DRUG RESISTANCE; ENZYMOLOGY; GENE AMPLIFICATION; GENETICS; HUMAN; ONCOGENE RAS; PATHOLOGY; SIGNAL TRANSDUCTION; TUMOR CELL LINE; UPREGULATION;

B RAF KINASE; BENZIMIDAZOLE DERIVATIVE; BRAF PROTEIN, HUMAN; KRAS PROTEIN, HUMAN; MITOGEN ACTIVATED PROTEIN KINASE KINASE; ONCOPROTEIN; PHOSPHATIDYLINOSITOL 3 KINASE; RAS PROTEIN; SELUMETINIB;

BENZIMIDAZOLES; CELL CYCLE; CELL DEATH; CELL LINE, TUMOR; COLORECTAL NEOPLASMS; DRUG RESISTANCE, NEOPLASM; GENE AMPLIFICATION; GENES, RAS; HUMANS; MAP KINASE SIGNALING SYSTEM; MITOGEN-ACTIVATED PROTEIN KINASE KINASES; PHOSPHATIDYLINOSITOL 3-KINASES; PROTO-ONCOGENE PROTEINS; PROTO-ONCOGENE PROTEINS B-RAF; RAS PROTEINS; UP-REGULATION;

EID: 79955399083     PISSN: 19450877     EISSN: 19379145     Source Type: Journal    
DOI: 10.1126/scisignal.4170er2     Document Type: Erratum

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