BCR-ABL- and Ras-independent activation of Raf as a novel mechanism of Imatinib resistance in CML

International Journal of Oncology

Volumn 39, Issue 3, 2011, Pages 585-591

  Hentschel, Julia ^a   Rubio, Ignacio ^a   Eberhart, Melanie ^a   Hipler, Christina ^a   Schiefner, Jana ^a   Schubert, Katrin ^a   Loncarevic, Ivan F ^a   Wittig, Ute ^a   Baniahmad, Aria ^a   Von Eggeling, Ferdinand ^a  

^a JENA UNIVERSITY HOSPITAL   (Germany)

Author keywords

Chronic myeloid leukemia; Imatinib; KCL22; MAPK; Raf; Signal transduction

Indexed keywords

2 MORPHOLINO 8 PHENYLCHROMONE; BCR ABL PROTEIN; GUANOSINE TRIPHOSPHATE; IMATINIB; MITOGEN ACTIVATED PROTEIN KINASE; RAF PROTEIN; RAPAMYCIN; RAS PROTEIN; WORTMANNIN;

ARTICLE; CHRONIC MYELOID LEUKEMIA; CONTROLLED STUDY; DRUG RESISTANCE; HUMAN; LEUKEMIA CELL; MUTATION; PHARMACOLOGICAL PARAMETERS; PRIORITY JOURNAL; PROTEIN FUNCTION; SEQUENCE ANALYSIS; SERUM;

BENZAMIDES; CELL GROWTH PROCESSES; CELL LINE, TUMOR; CLONE CELLS; DRUG RESISTANCE, NEOPLASM; ENZYME ACTIVATION; EXTRACELLULAR SIGNAL-REGULATED MAP KINASES; FUSION PROTEINS, BCR-ABL; HUMANS; LEUKEMIA, MYELOGENOUS, CHRONIC, BCR-ABL POSITIVE; MAP KINASE KINASE KINASES; PIPERAZINES; PROTEIN KINASE INHIBITORS; PYRIMIDINES; RAF KINASES; RAS PROTEINS;

EID: 79960001003     PISSN: 10196439     EISSN: 17912423     Source Type: Journal    
DOI: 10.3892/ijo.2011.1062     Document Type: Article

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