1 Professor of Hematology, Internal Medicine, Faculty of Medicine, Alexandria University, Egypt.
2 Professor of Pathology, Medical Genetics Center, Faculty of Medicine, Alexandria University, Egypt.
3 Professor of Clinical Pathology, Faculty of Medicine, Alexandria University, Egypt.
4 Hematology, Internal Medicine, Hematology Department, Faculty of Medicine, Taiz University, Yemen.
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Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm where
pathogenesis is based on the oncoprotein termed BCR‐ABL1. TET2
initiates DNA demethylation and is frequently mutated in hematological
malignancies, including CML. The relation between TET2 acquisition and
CML transformation and/or imatinib resistance is needed to be
Aim of Work
Materials and Method
|Table 1. TET2 single polymorphism patterns for the 3 positions among the three studied groups (CML, and control).|
|Figure 1. Distribution of Single Nucleotide Polymorphism Among the Studied Group.|
|Table 2. Comparison between prognostic factors in CML cases in chronic phase and TET2 polymorphism.|
|Table 3. Comparison between tet2 polymorphism and BCR ABL1 IS% in chronic phase CML.|
Conclusions and Recommendations