Single nucleotide polymorphism rs4961 in the adducin 1 gene is not associated with gastric cancer or preneoplastic cancer lesions

Agreda-Fernández,Mireya Yamel; Ruiz-Piñón,Karime; De La Torre-Guzmán,Samantha Rebeca; Perea-Díaz,Francisco Javier; Magaña-Torres,María Teresa; Ernesto,Prado-Montes De Oca; Sánchez-López,Josefina Yoaly

doi:10.3892/ol.2024.14588

Single nucleotide polymorphism rs4961 in the adducin 1 gene is not associated with gastric cancer or preneoplastic cancer lesions

Authors:
- Mireya Yamel Agreda-Fernández
- Karime Ruiz-Piñón
- Samantha Rebeca De La Torre-Guzmán
- Francisco Javier Perea-Díaz
- María Teresa Magaña-Torres
- Prado-Montes De Oca Ernesto
- Josefina Yoaly Sánchez-López
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Affiliations: Genetics Division, Western Biomedical Research Center, Mexican Social Security Institute, Guadalajara, Jalisco 44340, Mexico, Research and Development Department, Medical Cluster of Jalisco State Civil Association, Guadalajara, Jalisco 45040, Mexico
Published online on: July 24, 2024 https://doi.org/10.3892/ol.2024.14588
Article Number: 455
Copyright: © Agreda-Fernández et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Gastric cancer (GC) is the fourth most deadly cancer globally. The adducin 1 (ADD1) protein is involved in oncogenic signal transduction pathways in several types of cancer, and the rs4961 variant (c.1378 G>T, p.Gly460Trp) of the ADD1 gene is associated with salt‑sensitive hypertension, renal cell cancer and breast cancer susceptibility; however, it has not been investigated in GC. The aim of the present study was to evaluate the association between the rs4961 variant and the development of GC and preneoplastic gastric lesions (PGLs) in a population from western Mexico. A total of 225 individuals who underwent an endoscopy were evaluated, of which 71 patients had histopathologically diagnosed GC and 53 patients had PGLs, with 101 patients used as controls. The rs4961 variant was genotyped by using PCR and DNA sequencing. The frequency of the mutated homozygous genotype (TT) of the rs4961 variant was <10% in the three evaluated groups, and the frequency of the minor allele (T) was <21% in the GC, PGL and control groups. Genotypic and allelic frequencies were similarly distributed in all of the studied groups (P>0.05). In summary, in the study population, the rs4961 variant was not associated with GC risk; however, its role in other populations and in other types of cancer is worthy of future research.

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