- Helicobacter pylori, a gram-negative bacterium that colonizes the stomach lining, has long been recognized as a significant risk factor for gastric cancer.
- This infection is strongly associated with both major subtypes of gastric adenocarcinoma, intestinal-type and diffuse-type, though the strength and nature of this relationship differ between the two.
- The intestinal-type gastric cancer, in particular, exhibits a more pronounced connection with H. pylori, following a well-documented progression known as Correa’s cascade. This sequence begins with chronic gastritis, advances to atrophic gastritis, intestinal metaplasia, dysplasia, and culminates in adenocarcinoma.
- Strains of H. pylori carrying the CagA pathogenicity island are especially implicated in driving this process, highlighting the bacterium’s role as a key initiator in the development of intestinal-type gastric cancer.
- Research underscores the disparity in H. pylori’s association with the two cancer subtypes. Studies have shown that evidence of H. pylori infection is far more prevalent in intestinal-type cases, with one study reporting that 89.2% of patients with this subtype had detectable H. pylori in non-cancerous gastric tissue. In contrast, only 31.8% of diffuse-type cases showed similar evidence, suggesting that H. pylori plays a more direct and consistent role in intestinal-type gastric cancer.
- The bacterium’s virulence factors, such as CagA, contribute to chronic inflammation and cellular changes that pave the way for malignancy, particularly in the intestinal-type pathway. This marked difference emphasizes the need to distinguish between these subtypes when evaluating H. pylori’s oncogenic impact.
- While the association with diffuse-type gastric cancer is less robust overall, it becomes more significant in specific contexts, notably in early-onset cases. Younger patients diagnosed with diffuse-type cancer often harbor H. pylori infections with distinct genotypes, such as vacA s1/m1. This suggests that the bacterium’s influence on diffuse-type cancer may be tied to factors like patient age and the genetic makeup of the infecting strain.
- Unlike the intestinal-type, which follows a stepwise progression, diffuse-type cancer tends to arise more sporadically and is less dependent on the chronic inflammatory cascade driven by H. pylori. Nevertheless, the presence of certain bacterial strains in younger patients indicates that H. pylori remains a relevant risk factor across both subtypes, albeit with varying mechanisms and degrees of influence.
- The progression from H. pylori infection to gastric cancer is not inevitable and depends on a complex interplay of factors beyond the bacterium itself. Bacterial virulence, such as the presence of CagA, interacts with host genetic susceptibility and environmental influences like diet and smoking to determine cancer risk.
- Not all individuals infected with H. pylori develop gastric cancer, which underscores the multifactorial nature of this disease. However, early intervention offers hope: eradicating H. pylori, particularly in the initial stages of precancerous changes, has been shown to reduce the risk of gastric cancer significantly. This preventive potential highlights the importance of screening and treating H. pylori infections, especially in populations at higher risk for gastric adenocarcinoma.
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