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HEMATOLOGICAL MALIGNANCY

Bone marrow fibrosis may be an effective independent predictor of the ‘TKI drug response level’ in chronic myeloid leukemia

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Figures & data

Figure 1. Bone marrow (BM) fibrosis and dysplasia of the de novo CML patient before TKI treatment (A1 and A2). Fibrosis and dysplasia of bone BM have been healed due to the pharmacobiological effects of TKIs after 3 years of imatinib and 1 year of dasatinib treatment (B1 and B2).

Figure 1. Bone marrow (BM) fibrosis and dysplasia of the de novo CML patient before TKI treatment (A1 and A2). Fibrosis and dysplasia of bone BM have been healed due to the pharmacobiological effects of TKIs after 3 years of imatinib and 1 year of dasatinib treatment (B1 and B2).

Table 1. Baseline characteristics of chronic myeloid leukemia patients

Table 2. TKI drug disposition in patients with chronic myeloid leukemia

Table 3. Molecular response rates based on BCR-ABL monitoring via polymerase chain reaction (PCR) in chronic myeloid leukemia patients with and without bone marrow fibrosis

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