Stomach (gastric) cancer is one of the most prevalent and deadly cancers worldwide and most gastric cancers are adenocarcinomas. Based on prior research, there is an association betweenHelicobacter pylori(H. pylori) infection together with the frequency of duodenal ulcer, distal gastric adenocarcinoma, mucosa-associated lymphoid tissue (MALT) lymphoma, and antral gastritis.Helicobacter pylorivirulence and toxicity factors have been identified before that significantly influence the clinical outcomes ofH. pyloriinfection and gastric adenocarcinoma. However, it remains unclear exactly how different strains ofH. pyloriaffect gastric adenocarcinoma. Current research suggests this involves tumor suppressor genes, likep27but alsoH. pyloritoxic virulence proteins. Therefore, we quantified knownH. pylorigenotypes within adenocarcinoma patients to establish the prevalence of known toxins that include cytotoxin-associated gene A (cagA) as well as vacuolating cytotoxin A (vacA) within patients of variable adenocarcinoma diagnosis. This analysis used gastrectomy samples validated for DNA viability. The incidence ofH. pyloriin adenocarcinoma patients in Jordan was established to be 54.5% positive (ureAgene positive) with cagAgenotype occurrence at 57.1%, but also in this population study vacAgene ratios found to be 24.7%:22.1%:14.3%:14.3%. (vacAs1:vacAs2:vacAm1:vacAm2). Using immunohistochemistry (IHC), we confirmed with statistical significance that p27 was dysregulated and suppressed, within nearly allH. pylori vacAgenotypes. In addition, within 24.6% ofH. pylorisamples analyzed was a different bacterial genotype, and curiously that p27 protein expression was retained in 12% of tested adenocarcinomaH. pylorisamples. This is suggestive that p27 could be used as a prognostic indicator but also that an unknown genotype could be contributing to the regulatory effects of p27 protein within this bacterial and cellular environment that may include other virulence factors and unknown immune system regulatory changes.Supplementary InformationThe online version contains supplementary material available at 10.1007/s44197-023-00099-z.