| Literature DB >> 24262285 |
Hidehiro Itonaga1, Hideki Tsushima2, Daisuke Imanishi1, Tomoko Hata1, Yuko Doi3, Sayaka Mori3, Daisuke Sasaki3, Hiroo Hasegawa3, Emi Matsuo4, Jun Nakashima4, Takeharu Kato1, Makiko Horai1, Masataka Taguchi1, Masatoshi Matsuo1, Hiroaki Taniguchi1, Junnya Makiyama4, Shinya Sato4, Kensuke Horio4, Koji Ando1, Yuji Moriwaki4, Yasushi Sawayama1, Daisuke Ogawa4, Reishi Yamasaki4, Yumi Takasaki4, Yoshitaka Imaizumi1, Jun Taguchi1, Yasuhisa Kawaguchi4, Shinichiro Yoshida4, Tatsuro Joh4, Yukiyoshi Moriuchi4, Hiroaki Nonaka4, Hisashi Soda4, Takuya Fukushima5, Kazuhiro Nagai6, Shimeru Kamihira4, Masao Tomonaga4, Katsunori Yanagihara3, Yasushi Miyazaki1.
Abstract
An appropriate trigger for BCR-ABL1 mutation analysis has not yet been established in unselected cohorts of chronic-phase chronic myelogenous leukemia patients. We examined 92 patients after 12 months of tyrosine kinase inhibitor (TKI) treatment in Nagasaki Prefecture, Japan. Univariate analysis revealed that significant factors associated with not attaining a major molecular response (MMR) were the presence of the minor BCR-ABL1 fusion gene, a low daily dose of TKI, and the emergence of BCR-ABL1 kinase domain mutations conferring resistance to imatinib. Factors associated with the loss of sustained MMR were a low daily dose of TKI and the emergence of alternatively spliced BCR-ABL1 mRNA with a 35-nucleotide insertion. Taken together, our results suggest that the search for BCR-ABL1 mutations should be initiated if patients have not achieved MMR following 12 months of TKI treatment.Entities:
Keywords: Alternative splicing; BCR-ABL1; Chronic myelogenous leukemia; Mutation; Resistance
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Year: 2013 PMID： 24262285 DOI： 10.1016/j.leukres.2013.10.022
Source DB: PubMed Journal: Leuk Res ISSN： 0145-2126 Impact factor: 3.156