Japanese researchers have identified the process from which Helicobacter pylori, found in half of the world's population, can cause stomach cancer.
In 2017, 6,600 new cases of stomach cancer (also called gastric cancer) were diagnosed in France. In 65% of cases, patients are men, usually over 65 years old. Although the annual incidence of this cancer is much higher in some countries in Asia, Central Europe and Latin America, there is still an evolution of the disease with, for example, an increasing incidence of cardiac cancer. (junction with the esophagus).
The role of the bacteria Helicobacter pylori
In the majority of cases, the bacterium Helicobacter pylori is at the origin of the development of stomach cancer. This bacterium, classed in 1994 by IARC as a carcinogen class I, that is to say as a carcinogen certain for humans, infects the gastric mucosa and causes 80% of peptic 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 so far been unclear.
Japanese researchers from Kanazawa University and the Japanese Agency for Research and Development in Medicine 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 the formation of tumors by activating a protein called NOXO1, but we did not know how NOXO1 induces the formation of tumors 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 oxidative effect of these ROS results in mutations in the DNA of the cells of the stomach, leading to the formation of tumors. And the inflammation caused by a Helicobacter pylori also produces ROS, which increases oxidative stress in the stomach.
Researchers have shown that inflammation causes excessive expression of NOXO1 protein in response to a regulatory protein, NF-KB, which activates genes to fight stress and bacterial infections and is a major player in the inflammatory response. .
The growth of cancer cells stopped
They then used a drug on mice to suppress NOXO1 activity, which immediately stopped the growth of gastric cancer cells. "If we can disrupt in situ the NOXO1 / ROS signaling pathway, we may be able to prevent the development of this cancer," the authors conclude. But new studies must be conducted to deepen these results.