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

Pak J Biol Sci. 2022 Jan;25(2):175-181. doi: 10.3923/pjbs.2022.175.181.

Abstract

<b>Background and Objective:</b> 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. <b>Materials and Methods:</b> 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. <b>Results:</b> 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). <b>Conclusion:</b> 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.

Keywords: BCR-ABL T315I gene; Chronic myeloid leukaemia; chromosome; haematological parameters; mutation; tyrosine kinase.

MeSH terms

  • 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

Substances

  • Protein Kinase Inhibitors
  • Fusion Proteins, bcr-abl