Original Research Article The Egyptian Journal of Immunology Volume 29 (4), 2022: 163–173. www.Ejimmunology.org sVCAM-1, and TGFβ1 in chronic phase, chronic myeloid leukemia patients treated with tyrosine kinase inhibitors Muhamad R. Abdel Hammed 1 , Yoseryeia A. Ahmed 2 , Esraa N. Adam 2 , Rania Bakry 3 and Mohamed G. Elnaggar 3 1 Department of Internal Medicine & Hematology Unit, Assiut University Hospitals and South Egypt Cancer Institute Bone Marrow Transplantation Unit, Assiut University, Assiut, Egypt. 2 Department of Internal Medicine & Hematology Unit, Assiut University Hospitals, Assiut University, Assiut, Egypt. 3 Department of Clinical Pathology, South Egypt Cancer Institute, Assiut University, Assiut, Egypt. Corresponding author: Muhamad R. Abdel Hameed, Department of Internal Medicine, Hematology Unit, Assiut University Hospitals and South Egypt Cancer Institute Bone Marrow Transplantation Unit, Assiut University, Assiut, Egypt. Email: muhammadramadan@aun.edu.eg. dr.muhamadramadan@yahoo.com Abstract The outcome for chronic phase (CP) chronic myelogenous leukemia (CML) patients has changed dramatically since the introduction of tyrosine kinase inhibitor (TKI) therapy. We examined the characteristics of CML patients during TKI therapy by determining the plasma concentrations of soluble vascular cell adhesion molecule 1 (sVCAM-1), and transforming growth factor (TGFβ1) biomarkers. The plasma levels of sVCAM-1 and TGFβ1 were measured by ELISA at baseline and after 3 months of TKI treatment. The levels of sVCAM-1, and TGFβ1 were significantly elevated in patients with CML (P< 0.01). Dasatinib treatment was associated with a significant reduction in the levels of these biomarkers (P< 0.01). In conclusion, plasma levels of sVCAM-1 and TGFβ1 could have a role in the pathogenesis of CML and may be used as predictors of hematological and molecular responses to TKIs. A favorable outcome for Dasatinib therapy was observed. Keywords: CML, TKI, TGFβ1, sVCAM-1, Imatinib, Dasatinib, Nilotinib. Date received: 13 August 2022; accepted: 07 September 2022 Introduction Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm characterized by uncontrolled proliferation of immature myeloid cells in the bone marrow and organs. Also, it is characterized by blood leukocytosis by neutrophils in different stages of maturation. 1 Tyrosine-protein kinase ABL1 (ABL1) expression has increased in many cases of CML in patients with the fusion gene breakpoint cluster region-Abelson murine leukemia virus oncogene homolog 1 (BCR-ABL1). Tyrosine kinase inhibitors, as ABL1 inhibitors, are used for the treatment of CML patients. 2 First generation treatment Imatinib is advised for patients who are Sokal low risk while Nilotinib for Sokal intermediate or high risk without cardiovascular disease. In failure of