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Updated: Aug 17, 2026
Methyl-binding DNA capture Sequencing for Patient Tissues
Published on: October 31, 2016
CDKN2A promoter methylation in gastric adenocarcinomas: clinical variables
Q N Vo1, J Geradts, D A Boudreau
1Department of Pathology, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA.
Abstract:
The CDKN2A gene encodes a cyclin-dependent kinase inhibitor, p16, which promotes cell cycle arrest. Methylation of the promoter region of the gene transcriptionally inactivates the gene. We have analyzed the methylation status of the promoter region of the CDKN2A gene in gastric adenocarcinomas using methylation-specific polymerase chain reaction. We also examined the tumors by immunohistochemistry for p16 protein. Of 114 gastric adenocarcinomas analyzed by immunohistochemistry, 34 cases (30%) were negative for p16 protein. Twenty-four of these 34 cases (71%) had methylation of the promoter region of the CDKN2A gene. Methylation of the promoter was strongly associated with loss of p16 protein by immunohistochemistry (P <0.0001). Neither stage, grade, anatomic site, or histologic subtype of the tumor nor age, gender, ethnic origin, or survival time of the patient were significantly different between the groups characterized by tumors with and without methylation. CDKN2A promoter methylation was not significantly associated with microsatellite instability.
Insights
Methylation of the CDKN2A gene promoter inactivates the gene, leading to a loss of p16 protein in gastric cancer. This epigenetic change is strongly linked to p16 protein absence in tumors.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- The CDKN2A gene encodes p16, a protein crucial for cell cycle arrest.
- Promoter methylation of CDKN2A leads to transcriptional silencing.
- Gastric adenocarcinoma is a significant global health concern.
Purpose of the Study:
- To investigate the frequency and significance of CDKN2A promoter methylation in gastric adenocarcinomas.
- To correlate CDKN2A methylation status with p16 protein expression.
- To explore associations between CDKN2A methylation and clinicopathological features.
Main Methods:
- Analysis of CDKN2A promoter methylation using methylation-specific polymerase chain reaction.
- Immunohistochemical assessment of p16 protein expression in 114 gastric adenocarcinomas.
- Statistical analysis to determine correlations.
Main Results:
- CDKN2A promoter methylation was detected in a subset of gastric adenocarcinomas.
- Loss of p16 protein expression was observed in 30% of tumors.
- A strong association was found between CDKN2A promoter methylation and the absence of p16 protein (P <0.0001).
- No significant associations were found with tumor stage, grade, histology, patient demographics, or survival.
- CDKN2A methylation was not linked to microsatellite instability.
Conclusions:
- CDKN2A promoter methylation is a key mechanism for p16 silencing in gastric cancer.
- Epigenetic silencing of CDKN2A is strongly correlated with p16 protein loss.
- CDKN2A methylation status does not appear to be influenced by common clinicopathological factors or microsatellite instability in this cohort.
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