Investigating FGFR2 gene as a blood-based epigenetic biomarker in gastric cancer.

Autor: Aleyasin SA; Department of Medical Biotechnology, National Institute of Genetic Engineering and Biotechnology (NIGEB), 17 Km Tehran-Karaj Highway, Pajoohesh Blvd, Tehran, Iran. sogand@nigeb.ac.ir., Moradi A; Department of Medical Biotechnology, National Institute of Genetic Engineering and Biotechnology (NIGEB), 17 Km Tehran-Karaj Highway, Pajoohesh Blvd, Tehran, Iran., Abolhasani N; Department of Medical Biotechnology, National Institute of Genetic Engineering and Biotechnology (NIGEB), 17 Km Tehran-Karaj Highway, Pajoohesh Blvd, Tehran, Iran., Abdollahi M; Department of Medical Biotechnology, National Institute of Genetic Engineering and Biotechnology (NIGEB), 17 Km Tehran-Karaj Highway, Pajoohesh Blvd, Tehran, Iran.
Jazyk: angličtina
Zdroj: Molecular biology reports [Mol Biol Rep] 2024 Feb 01; Vol. 51 (1), pp. 253. Date of Electronic Publication: 2024 Feb 01.
DOI: 10.1007/s11033-023-09082-0
Abstrakt: Background: Gastric adenocarcinoma is a prevalent form of cancer that often remains undetected in its early stages due to the lack of specific symptoms. This delayed diagnosis leads to poor clinical outcomes, underscoring the need for an effective and non-invasive method for early detection. Recent advances in cancer epigenetics have led to the identification of biomarkers that have the potential to revolutionize the early detection and monitoring of this disease. One such promising biomarker is the methylation of the FGFR2 promoter. This study aims to measure the methylation levels of a specific CpG site in the FGFR2 promoter gene in DNA extracted from blood leukocytes from patients with intestinal metaplasia, gastric cancer, and healthy control.
Material and Methods: The CpG site of the FGFR2 gene promoter was identified in its control region. Methylation alteration of the selected FGFR2 CpG site was determined through the (methylation-sensitive restriction enzyme) MSRE-qPCR. Genomic DNA was extracted from one hundred twenty-five participants.
Results: The normal group had mean methylation levels of 93.23 ± 4.929%, while the IM group had a level of 69.85 ± 27.15%. In GC patients, the levels varied, with 25.96 ± 18.98% in the intestinal type and 28.30 ± 16.07% in the diffuse type. The methylation levels in the IM and GC patients were significantly lower than those in the normal control group. However, no significant difference was observed between the methylation status of the intestinal type of GC and the diffuse type. The Receiver operating characteristic (ROC) curve analysis showed that FGFR2 CpG methylation levels in GC patients compared to normal controls had a high sensitivity of 100% and specificity of 100%, with a cut-off of < 74.25%; when GC patients were compared to IM patients, the sensitivity was 85%, and the specificity was 80%, with a cut-off < 44.45%.
Conclusions: The potential of the FGFR2 methylation status as a non-invasive biomarker lies in its ability to be detected in blood leukocytes, which makes it a promising tool for the early detection of intestinal metaplasia and gastric cancer. This could significantly improve the detection and management of these gastric conditions.
(© 2024. The Author(s), under exclusive licence to Springer Nature B.V.)
Databáze: MEDLINE
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