Pandey Neetu, Yadav Geeta, Kushwaha Rashmi, Verma Shailendra Prasad, Singh Uma Shankar, Kumar Ashutosh, Mishra Prabhaker
Department of Pathology, King George's Medical University, Lucknow, U.P. 226003, India.
Department of Clinical Hematology, King George's Medical University, Lucknow, U.P. 226003, India.
Adv Hematol. 2019 Jan 1;2019:1835091. doi: 10.1155/2019/1835091. eCollection 2019.
Chronic myeloid leukemia (CML) is characterized by hyperproliferation of myeloid precursors, increased fibrosis, and neoangiogenesis in the bone marrow. Imatinib inhibits BCR-ABL tyrosine kinase produced due to reciprocal translocation t(9;22) in neoplastic CML cells. It reduces hyperproliferation of myeloid precursors and has been found to affect bone marrow fibrosis and angiogenesis. This study was done to assess the effect of imatinib on bone marrow morphology and angiogenesis in CML.
31 newly diagnosed CML patients were evaluated before and after 3 months of imatinib therapy. A marrow morphological response (MMR) score was used to assess marrow cytological and histological features including grade of fibrosis. Mean microvessel density (MVD) was also assessed. Hematological parameters and BCR-ABL transcript levels were assessed in the peripheral blood.
86.21% of patients showed decrease in marrow cellularity with normalization of M:E ratio. 72.42% of patients had decrease in grade of fibrosis and 17.24% showed no change while 10.34% of patients showed progression of fibrosis grade. Patients with MMR score ≥ 2 (n=4) and those with progression of fibrosis grade (n=3) showed suboptimal molecular response (BCR-ABL transcripts > 10%). Pretherapy mean MVD of patients (14.69 ± 5.28) was higher than that of controls (6.32 ± 1.64). A significant reduction of 66.51% was observed in posttherapy mean MVD (4.98 ± 2.77) of CML patients (p<0.001).
Imatinib therapy in CML not only decreases marrow cellularity, but also helps towards normalization of bone marrow microenvironment by reducing fibrosis and angiogenesis.
慢性髓性白血病（CML）的特征是骨髓中髓系前体细胞过度增殖、纤维化增加和新生血管形成。伊马替尼可抑制肿瘤性CML细胞中因相互易位t(9;22)产生的BCR-ABL酪氨酸激酶。它可减少髓系前体细胞的过度增殖，并已发现其可影响骨髓纤维化和血管生成。本研究旨在评估伊马替尼对CML患者骨髓形态和血管生成的影响。
对31例新诊断的CML患者在伊马替尼治疗3个月前后进行评估。采用骨髓形态学反应（MMR）评分来评估骨髓细胞学和组织学特征，包括纤维化程度。还评估了平均微血管密度（MVD）。对外周血中的血液学参数和BCR-ABL转录水平进行了评估。
86.21%的患者骨髓细胞数量减少，M:E比值恢复正常。72.42%的患者纤维化程度降低，17.24%无变化，而10.34%的患者纤维化程度进展。MMR评分≥2的患者（n = 4）和纤维化程度进展的患者（n = 3）显示分子反应欠佳（BCR-ABL转录本>10%）。患者治疗前的平均MVD（14.69±5.28）高于对照组（6.32±1.64）。CML患者治疗后的平均MVD（4.98±2.77）显著降低了66.51%（p<0.001）。
CML患者接受伊马替尼治疗不仅可减少骨髓细胞数量，还可通过减少纤维化和血管生成帮助骨髓微环境恢复正常。
