BRAF mutation: Supporting diversity in HCL

Blood

Volumn 119, Issue 14, 2012, Pages 3193-3194

  Burger, Jan A ^a  

^a UNIVERSITY OF TEXAS MD ANDERSON CANCER CENTER   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

B RAF KINASE; B RAF KINASE INHIBITOR; DACARBAZINE; VEMURAFENIB;

AMINO ACID SEQUENCE; CANCER DIAGNOSIS; CANCER SURVIVAL; CELL GROWTH; CLINICAL FEATURE; DISEASE COURSE; GENE MUTATION; GENE TARGETING; GENETIC VARIABILITY; HAIRY CELL LEUKEMIA; HUMAN; IMMUNOPHENOTYPING; MELANOMA; MELANOMA CELL; NOTE; OVERALL SURVIVAL; PATHOGENESIS; PRIORITY JOURNAL; PROGRESSION FREE SURVIVAL; WILD TYPE;

EID: 84859623264     PISSN: 00064971     EISSN: 15280020     Source Type: Journal    
DOI: 10.1182/blood-2012-01-403659     Document Type: Note

References (8)

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8. Villanueva J, Vultur A, Lee JT, et al. Acquired resistance to BRAF inhibitors mediated by a RAF kinase switch in melanoma can be overcome by cotargeting MEK and IGF-1R/PI3K. Cancer Cell. 2010;18(6):683-695.