Japanese researchers have identified the process by which the bacterium Helicobacter pylori, present in half of the world’s population, could be the cause of stomach cancer.
In 2017, 6,600 new cases of stomach cancer (also called gastric cancer) were diagnosed in France. In 65% of cases, the patients are men, generally over the age of 65. Although the annual incidence of this cancer is much higher in certain countries of Asia, Central Europe and Latin America, we are still observing an evolution of the disease with, for example, an increasing incidence of cardia cancer. (junction with the esophagus).
The role of bacteria Helicobacter pylori
In the majority of cases, the bacteria Helicobacter pylori causes the development of stomach cancer. This bacterium, classified in 1994 by the IARC as a class I carcinogen, ie as a definite carcinogen for humans, infects the gastric mucosa and causes 80% of gastro-duodenal ulcers. This bacterium is acquired during childhood, but persists throughout life. The occurrence of invasive stomach cancer occurs in 3% of people with Helicobacter pylori. In nearly 80% of cases, infected people are asymptomatic. Despite this knowledge, the precise way in which this bacterium facilitates the development of gastric cancer has until now remained unclear.
Japanese researchers from Kanazawa University and Japan’s Agency for Medical Research and Development may have found the answer. The results of their work have been published in the journal Oncogene. “We had shown that tumor necrosis factor TNF-alpha, a cytokine that causes inflammation, promotes tumor formation by activating a protein called NOXO1. But we did not know how NOXO1 induces tumor formation in the stomach,” explains Dr. Kanae Echizen, lead author of the study.
Mutations in the DNA of gastric cells
Specifically, NOXO1 produces molecules called Reactive Oxygen Species (ROS) that damage tissue. The oxidizing effect of these ROS in fact leads to mutations in the DNA of stomach cells, leading to the formation of tumours. And the inflammation caused by an infection Helicobacter pylori also produces ROS, which increases oxidative stress in the stomach.
The researchers showed that inflammation caused excessive expression of the NOXO1 protein in response to a regulatory protein, NF-KB, which activates genes to fight against stress and bacterial infections and which is a major player in the inflammatory response. .
Stopped cancer cell growth
They then used a drug on mice to suppress the activity of NOXO1, which immediately stopped the growth of gastric cancer cells. “If we can disrupt the NOXO1/ROS signaling pathway in-situ, we may be able to prevent the development of this cancer”, conclude the authors. However, further studies need to be conducted to explore these results further.
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