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Updated: Jun 1, 2025
Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance
Published on: March 7, 2025
Comparison of Genetic Mutations of Gastric Cancer Diagnosed before or after Helicobacter pylori Eradication and
Masaaki Kodama1,2, Manami Oda3, Kazuhiro Mizukami2
1Department of Advanced Medical Sciences, Faculty of Medicine, Oita University, Oita, Japan.
Introduction:
Genetic abnormalities specific to post-Helicobacter pylori eradication gastric cancer (GC), especially those associated with undifferentiated post-eradication GC, are unknown. We conducted next-generation sequencing of GC diagnosed either before or after eradication to investigate the carcinogenesis of post-eradication GC.
Methods:
Five cases of post-eradication differentiated GC [HP(-)-D group], five cases of H. pylori-positive differentiated GC [HP(+)-D group], four cases of post-eradication undifferentiated GC [HP(-)-U group], and six cases of H. pylori-positive undifferentiated GC [HP(+)-U group] underwent analysis. DNA was extracted from tumor samples, and non-tumor samples of all subjects. Next-generation target sequencing was conducted using the Ion AmpliSeq Library Kit 2.0 with the Ion AmpliSeq Cancer Hotspot Panel v2. Next-generation targeted sequencing results of the cancer part were subtracted from the results of the non-cancer part.
Results:
The HP(-)-D group displayed significantly fewer SNPs in hotspot than the other groups (p < 0.01). Definitive DNA mutations were identified by sequencing of cancerous and non-cancerous tissues. 5 of 20 patients had specific somatic mutations, with different TP53 mutations in the HP(+)-D and HP(-)-U groups, CTNNB1 mutations in the HP(+)-U group, and ATM mutations in the HP(+)-U group, but no mutations in the HP(-)-D group.
Conclusion:
Several definite genetic mutations involved in GC were observed. Mutations were less frequent in post-eradication differentiated GC. However, because of small number of cases analyzed to identify carcinogenic differences, further analysis with a large number of cases and with strictly grading GC samples is needed.
Introduction:
Genetic abnormalities specific to post-Helicobacter pylori eradication gastric cancer (GC), especially those associated with undifferentiated post-eradication GC, are unknown. We conducted next-generation sequencing of GC diagnosed either before or after eradication to investigate the carcinogenesis of post-eradication GC.
Methods:
Five cases of post-eradication differentiated GC [HP(-)-D group], five cases of H. pylori-positive differentiated GC [HP(+)-D group], four cases of post-eradication undifferentiated GC [HP(-)-U group], and six cases of H. pylori-positive undifferentiated GC [HP(+)-U group] underwent analysis. DNA was extracted from tumor samples, and non-tumor samples of all subjects. Next-generation target sequencing was conducted using the Ion AmpliSeq Library Kit 2.0 with the Ion AmpliSeq Cancer Hotspot Panel v2. Next-generation targeted sequencing results of the cancer part were subtracted from the results of the non-cancer part.
Results:
The HP(-)-D group displayed significantly fewer SNPs in hotspot than the other groups (p < 0.01). Definitive DNA mutations were identified by sequencing of cancerous and non-cancerous tissues. 5 of 20 patients had specific somatic mutations, with different TP53 mutations in the HP(+)-D and HP(-)-U groups, CTNNB1 mutations in the HP(+)-U group, and ATM mutations in the HP(+)-U group, but no mutations in the HP(-)-D group.
Conclusion:
Several definite genetic mutations involved in GC were observed. Mutations were less frequent in post-eradication differentiated GC. However, because of small number of cases analyzed to identify carcinogenic differences, further analysis with a large number of cases and with strictly grading GC samples is needed.
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