Description
Title: Imatinib’s impact on the morphology and angiogenesis of the bone marrow in chronic myeloid leukemia
Abstract: Background information and goals Hyperproliferation of myeloid precursors, increased fibrosis, and neoangiogenesis in the bone marrow are characteristics of chronic myeloid leukemia (CML). Imatinib blocks the BCR-ABL tyrosine kinase that is produced in malignant CML cells as a result of the reciprocal translocation t(9;22). It has been discovered that it affects bone marrow fibrosis and angiogenesis, as well as reducing hyperproliferation of myeloid precursors. Imatinib’s impact on bone marrow morphology and angiogenesis in CML was evaluated in this study. Methods. Before and after receiving imatinib treatment for three months, 31 patients with recently discovered CML were assessed. The grade of fibrosis and other marrow cytological and histological features were evaluated using a marrow morphological response (MMR) score. Also evaluated was mean microvessel density (MVD). In the peripheral blood, BCR-ABL transcript levels and hematological parameters were evaluated. Results. 86.21% of patients had decreased marrow cellularity as the M:E ratio returned to normal. 72.42% of patients experienced a decline in fibrosis grade, 17.24% showed no change, and 10.34% of patients experienced fibrosis grade progression. The number of patients (n=4) with an MMR score below two and the number (n=3) with fibrosis grade progression showed suboptimal molecular responses (BCR-ABL transcripts > 10%). Pretherapy mean MVD was higher in patients (14.69 5.28) than in controls (6.32 1.64). The posttherapy mean MVD (4.98 2.77) of CML patients significantly decreased by 66.51% (p 0.001). Conclusion. In addition to lowering marrow cellularity in CML patients, imatinib therapy also contributes to the normalization of the bone marrow microenvironment by lowering fibrosis and angiogenesis.
Paper Quality: SCOPUS / Web of Science Level Research Paper
Subject: Medicine
Sub Category: Hematology
Writer Experience: 20+ Years
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