ArticleMolecular biology reports2025
Novel and recurrent mutations in exon 8 of natural killer group 2D (NKG2D) gene among chronic myeloid leukemia patients and their potential role in pathogenesis.
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- Treatment-Free Remission in Chronic Myeloid Leukemia: Toward Precision and Personalized Approaches to Functional Cure.Cancer science · 2026Review
- Honeybee venom modulates antioxidant gene expression and tissue regeneration in a rat model of staphylococcus aureus - infected skin wounds.Molecular biology reports · 2026Article
- Molecular analysis of FSHR rs6166 polymorphism and oxidative stress parameters in women with polycystic ovary syndrome.Molecular biology reports · 2026Article
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Abstract
backgroundMutations in NKG2D gene increase the risk of cancer, including chronic myeloid leukemia (CML). The Mutational landscape of exon 8 of NKG2D gene remains poorly characterized, especially in CML. PURPOSE: Exploring the mutations in exon 8 of NKG2D gene of CML patients, examine its interactions with other genes, and evaluate associated biochemical, hematological and clinical-pathological parameters. METHODOLOGY: Blood samples from CML patients and healthy controls were collected for molecular, biochemical and hematological assessments. Mutations in exon 8 of NKG2D gene were detected using Sanger sequencing. NKG2D gene interactions were predicted via GeneMANIA database.
resultsin exon 8 of the NKG2D gene, mutations (substitution and deletion) were detected in 88% of CML patients, with 50% carrying multiple variants. Nine single nucleotide polymorphisms (SNPs) were identified, including eight substitutions and one deletion. The most frequent substitution was G > GC and six variants were novel. Homozygous 414G > C had the highest mutation score. GeneMANIA analysis revealed strong interactions between NKG2D and 20 other genes, notably HCST gene, with co-expression and pathway interactions involving thirteen and eleven genes, respectively. LDH levels were significantly higher in patients, while uric acid levels showed no significant difference. CML patients also had higher MID% and lower RBC count, hemoglobin and hematocrit levels. In addition, there were no statistically significant correlations between mutation burden and biochemical/hematological parameters.
conclusionNKG2D exon 8 mutations are highly prevalent among CML patients, with multiple or novel variants identified. A strong interaction profile of NKG2D with immune-related genes, indicating possible roles in leukemogenesis.
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