Prevalence of BCR-ABL T315I Mutation in Different Chronic Myeloid Leukemia patients Categories

Background and Objective: Chronic Myelogenous Leukaemia (CML) is a clonal myeloproliferative tumor distinguished by the existence of the Philadelphia chromosome (Ph) resulting from the t (9, 22) (q34, q11) translocation. The BCR-ABL gene and the fusion protein, which has constitutive tyrosine kinase...

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Published inPakistan journal of biological sciences : PJBS Vol. 25; no. 2; p. 175
Main Authors Elsir Khair, Hala, Ahmed Mohamed, Babker, Yousef Nour, Bakri, Ali Waggiallah, Hisham
Format Journal Article
LanguageEnglish
Published Pakistan 01.01.2022
Subjects
Cross-Sectional Studies
Drug Resistance, Neoplasm - genetics
Fusion Proteins, bcr-abl
Humans
Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy
Leukemia, Myelogenous, Chronic, BCR-ABL Positive - epidemiology
Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics
Mutation
Prevalence
Protein Kinase Inhibitors - pharmacology
mutation
haematological parameters
chromosome
tyrosine kinase
Chronic myeloid leukaemia
BCR-ABL T315I gene
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Summary:Background and Objective: Chronic Myelogenous Leukaemia (CML) is a clonal myeloproliferative tumor distinguished by the existence of the Philadelphia chromosome (Ph) resulting from the t (9, 22) (q34, q11) translocation. The BCR-ABL gene and the fusion protein, which has constitutive tyrosine kinase activity, are the outcome of this translocation. The purpose of this study is to determine the prevalence of the BCR-ABL T315I mutation in CML patients. Materials and Methods: Descriptive cross-sectional studies were conducted on 100 CML patients who visited RICK hospital between May, 2018-2019. T315I mutation analysis was done on all patients utilizing (RT/PCR) followed by RLFP to quantify the prevalence of Kinase Domain Mutation analysis (KDM) in CML. Results: The link between haematological parameters and ABL mutations in CML patients was shown to be a substantial positive correlation between T315I and haematological parameters (HB and WBC) but no correlation with PLT. The data revealed that 43 out of 99 CML had T315I, with highly prevalent gene express (43.4%) detected in all CML 56.6%. The correlation of T315I mutations with clinical status was positive significant (p-000). Conclusion: It can be concluded that T315I mutation became significantly higher in CML patients than in other groups of mutations. The detection of ABL kinase domain mutations may be a proper and valuable strategy for optimizing therapeutic methods and preventing treatment delays.
ISSN:1812-5735