Nilotinib in Imatinib-Resistant CML and Philadelphia Chromosome–Positive ALL
Author(s) -
Hagop M. Kantarjian,
Francis J. Giles,
Lydia Wunderle,
Kapil N. Bhalla,
Susan O’Brien,
Barbara Waßmann,
Chiaki Tanaka,
Paul W. Manley,
P. Rae,
William Mietlowski,
Kathy Bochinski,
Andreas Hochhaus,
James D. Griffin,
Dieter Hoelzer,
Maher Albitar,
Margaret Dugan,
Jorge E. Cortés,
Leila Alland,
Oliver G. Ottmann
Publication year - 2006
Publication title -
new england journal of medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 19.889
H-Index - 1030
eISSN - 1533-4406
pISSN - 0028-4793
DOI - 10.1056/nejmoa055104
Subject(s) - nilotinib , medicine , imatinib , imatinib mesylate , chronic myelogenous leukemia , tyrosine kinase inhibitor , adverse effect , philadelphia chromosome , pharmacology , leukemia , gastroenterology , oncology , myeloid leukemia , cancer , chromosomal translocation , gene , biochemistry , chemistry
Resistance to imatinib mesylate can occur in chronic myelogenous leukemia (CML). Preclinical in vitro studies have shown that nilotinib (AMN107), a new BCR-ABL tyrosine kinase inhibitor, is more potent than imatinib against CML cells by a factor of 20 to 50.
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