| ORIGINAL ARTICLE |
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| Year : 2018 | Volume
: 43
| Issue : 4 | Page : 171-178 |
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Role of circulating endothelial cells and platelet microparticles as markers of angiogenesis in chronic myeloid leukemia
Asmaa Nafady1, Mostafa F. Mohammed Saleh2, Hanaa Nafady-Hego3, Mohammed M Wahman4, Khalid A Nasif5, Wael F Sedik5
1 Department of Clinical Pathology, Faculty of Medicine, Assiut University, Assiut; Department of Clinical and
Chemical Pathology, South Valley University, Qena, Egypt
2 Clinical Hematology Unit, Internal Medicine Department, Faculty of Medicine, Assiut University, Assiut, Egypt
3 Department of Microbiology and Immunology, Faculty of Medicine, Assiut University, Assiut, Egypt
4 Department of Clinical Oncology, Qena Faculty of Medicine, Qena University Hospital, South Valley University, Qena, Egypt
5 Department of Medical Biochemistry and Molecular Biology, Faculty of Medicine, Minia University, Minia, Egypt
Correspondence Address:
Asmaa Nafady
Clinical Pathology Department, Assiut University, Assiut 71526
Egypt
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/ejh.ejh_22_18
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Background Circulating endothelial cells (CECs) and platelet microparticles (PMPs) are proposed as useful biosensors for angiogenesis and membrane damage in cancer. Moreover, PMPs can modulate cellular and humoral immunity.
Objective To measure CEC and PMP levels in patients with chronic myeloid leukemia (CML) with and without imatinib therapy.
Patients and methods Peripheral blood samples were obtained from 30 patients with CML at diagnosis (group A), 30 patients with CML on imatinib therapy of at least 1 year (group B), and 20 healthy controls (group C). Flow cytometry techniques were used to quantify CEC and PMP levels.
Results PMP percentage significantly increased in groups A and B when compared with group C (P=0.001 and 0.001, respectively). Mean±SEM of groups A, B, and C was 48.67±2.88, 42.50±2.82, and 22.70±1.18, respectively. There was an increased number of CECs in group A and B when compared with controls (P=0.001 and 0.001, respectively). Mean±SEM of groups A, B, and C was 149.33±23.82, 70.96±9.58, and 22.70±1.18, respectively. Patients with advanced phase or higher risk disease had slightly more PMPs and CECs than patients with chronic phase or low risk. Patients on imatinib therapy who achieved a complete molecular response at 1 year showed fewer PMPs and CECs.
Conclusion Higher PMPs and CECs number in patients with CML at diagnosis could indicate their pathogenic role as angiogenesis markers. However, their role of being prognostic factors and predictors of response to therapy in CML needs larger prospective studies.
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