Table of Contents Author Guidelines Submit a Manuscript
BioMed Research International
Volume 2016, Article ID 8086398, 9 pages
Research Article

Assessment of the Number and Phenotype of Macrophages in the Human BMB Samples of CML

1Department of Clinical Laboratory, Yunnan Provincial First People’s Hospital, Kunming, Yunnan 650032, China
2Institute of Clinical and Basic Medical Sciences, Yunnan Provincial First People’s Hospital, Kunming, Yunnan 650032, China
3Department of Hematology, Yunnan Provincial First People’s Hospital, Kunming, Yunnan 650032, China

Received 8 August 2016; Revised 24 October 2016; Accepted 3 November 2016

Academic Editor: Paul M. Tulkens

Copyright © 2016 Jian-Xin Song et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Macrophages have emerged as a key player in tumor biology. However, their number and phenotype in human bone marrow of biopsy (BMB) samples of chronic myeloid leukemia (CML) and their association with disease progression from an initial chronic phase (CP) to accelerated phase (AP) to advanced blast phase (BP) are still unclear. BMB samples from 127 CML patients and 30 patients with iron-deficiency anemia (IDA) as control group were analyzed by immunohistochemistry. The expression levels of CD68, CD163, and CD206 in BMB samples of CML patients were significantly higher than those in the patients of control group (), and we observed that their positive expression was gradually elevated during the transformation of CML-CP to AP to BP (). However, the expressions of CD68, CD163, and CD206 in released group were downregulated and contrasted to these in control group; there exists statistical significance (). The percentage ratio of CD163 and CD206 to CD68 was pronounced to be increasing from CML-CP to AP to BP (). Hence, the higher proportion of CD68+, CD163+ and CD206+ macrophages in BMB samples can be considered a key factor for disease progression of CML patients. Targeting macrophages, especially the M2 phenotype may help in designing therapeutic strategies for CML.