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BACKGROUND The resistance rate to antibacterial drugs is the key inhibitor of Helicobacter pylori ( H . pylori ) eradication treatment. AIM To evaluate the prevalence and drug resistance of H . pylori based on big data. METHODS Gastric mucosal specimens were collected from naive patients undergoing upper gastrointestinal endoscopy for H . pylori culture and antimicrobial susceptibility testing (AST), including clarithromycin, levofloxacin, metronidazole and amoxicillin. Every 10 years of age was grouped as an age group. The H . pylori infection and resistance were explored based on the age group and gender. RESULTS The number of H . pylori -positive specimen was 94509 in 283823 gastric mucosal specimens, with an infection rate of 33.30%. The infection rate increased with age, and males had a higher infection rate than females. The average resistance rate of H . pylori to amoxicillin and metronidazole was 0.21% and 93.72%, which remained stable. The average resistance rate to clarithromycin was 23.99% with an increasing trend from 14.43% to 38.24%. The average resistance rate to levofloxacin was 30.29%, which increased from 17.07% to 39.42% and mostly stabilized after 2017. The resistance rate of H . pylori increased with age, except amoxicillin. H . pylori in females are at higher risk of resistance to metronidazole, but not to amoxicillin, regardless of the age group. Meanwhile, H . pylori in females are at higher risk of resistance to levofloxacin and clarithromycin in the 21-50 age group. The single, dual, triple and quadruple-drug resistance rate was 54.59%, 29.03%, 11.71% and 0.11%, respectively. CONCLUSION The resistance of H . pylori in Taizhou city is serious. Guided by the consensus report, individualized treatment based on AST is recommended.

BACKGROUND Gastric cancer (GC), a multifactorial disease, is caused by pathogens, such as Helicobacter pylori ( H. pylori ) and Epstein-Barr virus (EBV), and genetic components. AIM To investigate microbiomes and host genome instability by cost-effective, low-coverage whole-genome sequencing, as biomarkers for GC subtyping. METHODS Samples from 40 GC patients were collected from Taizhou Hospital, Zhejiang Province, affiliated with Wenzhou Medical University. DNA from the samples was subjected to low-coverage whole-genome sequencing with a median genome coverage of 1.86 × (range: 1.03 × to 3.17 ×) by Illumina × 10, followed by copy number analyses using a customized bioinformatics workflow ultrasensitive chromosomal aneuploidy detector. RESULTS Of the 40 GC samples, 20 (50%) were found to be enriched with microbiomes. EBV DNA was detected in 5 GC patients (12.5%). H. pylori DNA was found in 15 (37.5%) patients. The other 20 (50%) patients were found to have relatively higher genomic instability. Copy number amplifications of the oncogenes, ERBB2 and KRAS, were found in 9 (22.5%) and 7 (17.5%) of the GC samples, respectively. EBV enrichment was found to be associated with tumors in the gastric cardia and fundus. H. pylori enrichment was found to be associated with tumors in the pylorus and antrum. Tumors with elevated genomic instability showed no localization and could be observed in any location. Additionally, H. pylori- enriched GC was found to be associated with the Borrmann type II/III and gastritis history. EBV-enriched GC was not associated with gastritis. No statistically significant correlation was observed between genomic instability and gastritis. Furthermore, these three different molecular subtypes showed distinct survival outcomes ( P = 0.019). EBV-positive tumors had the best prognosis, whereas patients with high genomic instability (CIN+) showed the worst survival. Patients with H. pylori infection showed intermediate prognosis compared with the other two subtypes. CONCLUSION Thus, using low-coverage whole-genome sequencing, GC can be classified into three categories based on disease etiology; this classification may prove useful for GC diagnosis and precision medicine.