MIR124-3 and NKX6-1 hypermethylation profiles accurately predict metachronous gastric lesions in a Caucasian population.


Journal

Clinical epigenetics
ISSN: 1868-7083
Titre abrégé: Clin Epigenetics
Pays: Germany
ID NLM: 101516977

Informations de publication

Date de publication:
21 Aug 2024
Historique:
received: 11 06 2024
accepted: 23 07 2024
medline: 22 8 2024
pubmed: 22 8 2024
entrez: 21 8 2024
Statut: epublish

Résumé

Early gastric cancer is treated endoscopically, but patients require surveillance due to the risk of metachronous gastric lesions (MGLs). Epigenetic alterations, particularly aberrant DNA methylation in genes, such as MIR124-3, MIR34b/c, NKX6-1, EMX1, MOS and CDO1, have been identified as promising biomarkers for MGL in Asian populations. We aimed to determine whether these changes could predict MGL risk in intermediate-risk Caucasian patients. This case-cohort study included 36 patients who developed MGL matched to 48 patients without evidence of MGL in the same time frame (controls). Multiplex quantitative methylation-specific PCR was performed using DNA extracted from the normal mucosa adjacent to the primary lesion. The overall risk of progression to MGL was assessed using Kaplan-Meier and Cox proportional hazards model analyses. MIR124-3, MIR34b/c and NKX6-1 were successfully analyzed in 77 samples. MIR124-3 hypermethylation was detected in individuals who developed MGL (relative quantification 78.8 vs 50.5 in controls, p = 0.014), particularly in females and Helicobacter pylori-negative patients (p = 0.021 and p = 0.0079, respectively). This finding was further associated with a significantly greater risk for MGL development (aHR = 2.31, 95% CI 1.03-5.17, p = 0.042). Similarly, NKX6-1 was found to be hypermethylated in patients with synchronous lesions (relative quantification 7.9 vs 0.0 in controls, p = 0.0026). A molecular-based methylation model incorporating both genes was significantly associated with a threefold increased risk for MGL development (aHR = 3.10, 95% CI 1.07-8.95, p = 0.037). This preliminary study revealed an association between MIR124-3 and NKX6-1 hypermethylation and the development of MGL in a Western population. These findings may represent a burden reduction and a greener approach to patient care.

Sections du résumé

BACKGROUND BACKGROUND
Early gastric cancer is treated endoscopically, but patients require surveillance due to the risk of metachronous gastric lesions (MGLs). Epigenetic alterations, particularly aberrant DNA methylation in genes, such as MIR124-3, MIR34b/c, NKX6-1, EMX1, MOS and CDO1, have been identified as promising biomarkers for MGL in Asian populations. We aimed to determine whether these changes could predict MGL risk in intermediate-risk Caucasian patients.
METHODS METHODS
This case-cohort study included 36 patients who developed MGL matched to 48 patients without evidence of MGL in the same time frame (controls). Multiplex quantitative methylation-specific PCR was performed using DNA extracted from the normal mucosa adjacent to the primary lesion. The overall risk of progression to MGL was assessed using Kaplan-Meier and Cox proportional hazards model analyses.
RESULTS RESULTS
MIR124-3, MIR34b/c and NKX6-1 were successfully analyzed in 77 samples. MIR124-3 hypermethylation was detected in individuals who developed MGL (relative quantification 78.8 vs 50.5 in controls, p = 0.014), particularly in females and Helicobacter pylori-negative patients (p = 0.021 and p = 0.0079, respectively). This finding was further associated with a significantly greater risk for MGL development (aHR = 2.31, 95% CI 1.03-5.17, p = 0.042). Similarly, NKX6-1 was found to be hypermethylated in patients with synchronous lesions (relative quantification 7.9 vs 0.0 in controls, p = 0.0026). A molecular-based methylation model incorporating both genes was significantly associated with a threefold increased risk for MGL development (aHR = 3.10, 95% CI 1.07-8.95, p = 0.037).
CONCLUSIONS CONCLUSIONS
This preliminary study revealed an association between MIR124-3 and NKX6-1 hypermethylation and the development of MGL in a Western population. These findings may represent a burden reduction and a greener approach to patient care.

Identifiants

pubmed: 39169394
doi: 10.1186/s13148-024-01712-z
pii: 10.1186/s13148-024-01712-z
doi:

Substances chimiques

MicroRNAs 0
Homeodomain Proteins 0
NKX6-1 protein, human 0
Biomarkers, Tumor 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

113

Subventions

Organisme : Fundação para a Ciência e a Tecnologia
ID : UI/BD/151488/2021
Organisme : HORIZON EUROPE Health
ID : 101095359
Organisme : UK Research and Innovation
ID : 10058099

Informations de copyright

© 2024. The Author(s).

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Auteurs

Catarina Lopes (C)

Precancerous Lesions and Early Cancer Management Group, Research Center of IPO Porto (CI-IPOP)/CI-IPOP@RISE (Health Research Group), Portuguese Institute of Oncology of Porto (IPO Porto)/Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC), Rua Dr. António Bernardino de Almeida, 4200-072, Porto, Portugal.
Center for Health Technology and Services Research (CINTESIS@RISE), University of Porto, Porto, Portugal.
School of Medicine and Biomedical Sciences (ICBAS), University of Porto, Porto, Portugal.

Tatiana C Almeida (TC)

Precancerous Lesions and Early Cancer Management Group, Research Center of IPO Porto (CI-IPOP)/CI-IPOP@RISE (Health Research Group), Portuguese Institute of Oncology of Porto (IPO Porto)/Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC), Rua Dr. António Bernardino de Almeida, 4200-072, Porto, Portugal.

Catarina Macedo-Silva (C)

Cancer Biology and Epigenetics Group, Research Center of IPO Porto (CI-IPOP)/CI-IPOP@RISE (Health Research Group), Portuguese Institute of Oncology of Porto (IPO Porto)/Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC), Porto, Portugal.

João Costa (J)

Department of Pathology, Portuguese Institute of Oncology of Porto, Porto, Portugal.

Sofia Paulino (S)

Department of Pathology, Portuguese Institute of Oncology of Porto, Porto, Portugal.

Carmen Jerónimo (C)

Cancer Biology and Epigenetics Group, Research Center of IPO Porto (CI-IPOP)/CI-IPOP@RISE (Health Research Group), Portuguese Institute of Oncology of Porto (IPO Porto)/Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC), Porto, Portugal.
Department of Pathology and Molecular Immunology, School of Medicine and Biomedical Sciences (ICBAS), University of Porto, Porto, Portugal.

Diogo Libânio (D)

Precancerous Lesions and Early Cancer Management Group, Research Center of IPO Porto (CI-IPOP)/CI-IPOP@RISE (Health Research Group), Portuguese Institute of Oncology of Porto (IPO Porto)/Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC), Rua Dr. António Bernardino de Almeida, 4200-072, Porto, Portugal.
Department of Gastroenterology, Portuguese Institute of Oncology of Porto, Porto, Portugal.

Mário Dinis-Ribeiro (M)

Precancerous Lesions and Early Cancer Management Group, Research Center of IPO Porto (CI-IPOP)/CI-IPOP@RISE (Health Research Group), Portuguese Institute of Oncology of Porto (IPO Porto)/Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC), Rua Dr. António Bernardino de Almeida, 4200-072, Porto, Portugal.
Department of Gastroenterology, Portuguese Institute of Oncology of Porto, Porto, Portugal.

Carina Pereira (C)

Precancerous Lesions and Early Cancer Management Group, Research Center of IPO Porto (CI-IPOP)/CI-IPOP@RISE (Health Research Group), Portuguese Institute of Oncology of Porto (IPO Porto)/Porto Comprehensive Cancer Center Raquel Seruca (Porto.CCC), Rua Dr. António Bernardino de Almeida, 4200-072, Porto, Portugal. ana.martins.pereira@ipoporto.min-saude.pt.

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