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文献和实验Fluorescence In Situ Hybridization for BCR-ABL
The BCR-ABL fusion gene arises as a result of a reciprocal translocation between chromosomes 9 and 22, resulting in the so-called Philadelphia (Ph) chromosome (a minute chromosome 22), which is found in 95% of cases of chronic myeloid
The use of oligodeoxynucleotides (ODN) to disrupt gene function has been studied in a variety of in vitro and in vivo systems (1 –14 ). Antigene, antisense, ribozyme, and aptamer nucleic acid molecules have been shown in numerous model
Detection of BCR-ABL Mutations and Resistance to Imatinib Mesylate
The major mechanism of imatinib resistance for patients with chronic myeloid leukemia (CML) is clonal expansion of leukemic cells with mutations in the Bcr-Abl fusion tyrosine kinase that reduce the capacity of imatinib to inhibit kinase
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