Impact of methionine synthase reductase polymorphisms in chronic myeloid leukemia patients

Abozer Y. Elderdery, Entesar M. Tebein, Fawaz O. Alenazy, Ahmed M. E. Elkhalifa, Manar G. Shalabi, Anass M. Abbas, Hassan H. Alhassan, Chand B. Davuljigari, Jeremy Mills

Research output: Contribution to journalArticlepeer-review

42 Downloads (Pure)


Introduction: Metabolism methionine and of folate play a vital function in cellular methylation reactions, DNA synthesis and epigenetic process. However, polymorphisms of methionine have received much attention in recent medical genetics research.

Objectives: To ascertain whether the common polymorphisms of the MTRR (Methionine Synthase Reductase) A66G gene could play a role in affecting susceptibility to Chronic Myeloid Leukemia (CML) in Sudanese individuals.

Methods: In a case-controlled study, we extracted and analyzed DNA from 200 CML patients and 100 healthy control subjects by the PCR-RFLP method.

Results: We found no significant difference in age or gender between the patient group and controls. The MTRR A66G genotypes were distributed based on the Hardy-Weinberg equilibrium (p > 0.05). The variation of MTRR A66G was less significantly frequent in cases with CML (68.35%) than in controls (87%) (OR = 0.146, 95% CI = 0.162–0.662, p < 0.002). Additionally, AG and GG genotypes and G allele were reducing the CML risk (Odds ratio [OR] = 0.365; 95% CI [0.179–0.746]; p = 0.006; OR = 0.292; 95% CI [0.145–0.590]; p = 0.001 and OR = 0.146; 95% CI [0.162–0.662]; p = 0.002 and OR = 2.0; 95% CI [1.3853–2.817]; respectively, (p = 0.000)).

Conclusions: Our data demonstrated that heterozygous and homozygous mutant genotypes of MTRR polymorphisms were associated with decreased risk of developing CML in the Sudanese population.
Original languageEnglish
Article number1729
Number of pages8
Issue number10
Publication statusPublished - 26 Sept 2022


  • CML
  • MTRR
  • folate and genetic polymorphism
  • Sudanese population


Dive into the research topics of 'Impact of methionine synthase reductase polymorphisms in chronic myeloid leukemia patients'. Together they form a unique fingerprint.

Cite this