Eliminating common bacterial infection significantly decreases gastric cancer risk
(University of Pennsylvania School of Medicine) Penn researchers are first to assess Helicobacter pylori infection and gastric cancer risk in Americans, certain demographics and ethnic groups.
Conclusion: Ten-day STT was more effective than 7-day STT for HP eradication. The eradication rate was not affected by the CYP2C19 genotype.
Background: Development of gastric diseases like gastritis, peptic ulcer and gastric cancer depends on several biotic and abiotic factors and Helicobacter pylori infection is a well-known biotic factor. However, not all H. pylori-infectedindividuals develop gastric diseases and not all individuals with gastric diseases are infected with H. pylori. Therefore, it is possible that other gastric bacteria also contribute to the formation and progression of gastric diseases.
ConclusionIn conclusion, all these data show thatH. pylori-induced autophagy is implicated in gastric CSC emergence and could represent an interesting therapeutic target.
Future Oncology,Volume 16, Issue 26, Page 1997-2006, September 2020.
ConclusionsCAM-resistantH. pylori was prevalent in one-third of patients in the Tokyo metropolitan area. VPZ-based triple therapy was highly effective and well-tolerated irrespective of CAM susceptibility. Therefore, it could be a valuable first-line treatment regimen forH. pylori infection.
Abstract SOURCE CITATION: Ford AC, Yuan Y, Moayyedi P. Helicobacter pylori eradication therapy to prevent gastric cancer: systematic review and meta-analysis. Gut. 2020. [Epub ahead of print]. 32205420. PMID: 32926811 [PubMed - as supplied by publisher]
ConclusionThe bacterium has various virulence factors, including cytotoxin- associated gene A, vacuolating cytotoxin A, and the different outer membrane proteins that cause cancer by different mechanisms. These virulence factors activate cell signaling pathways such as PI3-kinase/Akt, JAK/STAT and Ras, Raf, and ERK signaling that control cell proliferation. Uncontrolled proliferation can lead to cancer.
AbstractObjectiveIt remains unknown whether individuals with a family history (FH) of gastric cancer (GC) are associated with aberrant DNA methylation. The aim of this study was to investigate the association between aberrant DNA methylation and FH of GC.DesignUsing quantitative MethyLight assay,MOS,miR124a-3,NKX6-1,EMX1,CDH1, andTWIST1 methylation levels in the noncancerous gastric mucosa was compared between subjects with and without FH based on GC andHelicobacter pylori (Hp) infection. Changes in the methylation levels were evaluated over time after Hp eradication.ResultsIn Hp-positive GC patients,MOS (P
AbstractGastric cancer remains a major unmet clinical problem with over 1 million new cases worldwide. It is the fourth most commonly occurring cancer in men and the seventh most commonly occurring cancer in women. A major fraction of gastric cancer has been linked to variety of pathogenic infections including but not limited to Helicobacter pylori (H. pylori) or Epstein Barr virus (EBV). Strategies are being pursued to prevent gastric cancer development such asH. pylori eradication, which has helped to prevent significant proportion of gastric cancer. Today, treatments have helped to manage this disease and the 5-year sur...
The pathogenesis ofHelicobacter pylori-associated gastric cancer is dependent on delivery of CagA into host cells through a type IV secretion system (T4SS). TheH. pylori Cag T4SS includes a large membrane-spanning core complex containing 5 proteins, organized into an outer membrane cap (OMC), a periplasmic ring (PR) and a stalk. Here, we report cryo-EM reconstructions of a core complex lacking Cag3 and an improved map of the wild-type complex. We define the structures of two unique species-specific components (Cag3 and CagM) and show that Cag3 is structurally similar to CagT. Unexpectedly, components of the OMC are organiz...