AMOR Vol. 2, Issue 3, 2016

Abstract

astric cancer is a significant cause of cancer-related mortality and morbidity. In terms of disease etiology, it ranks as the fourth and fifth most common contributor of male and female cancer-related death, respectively [1] . A marked geographical variability has been observed for gastric cancer incidence, with the majority of cases reported in Eastern Europe, South America, and Asia [2] . This has been ascribed to environmental (e.g., H. pylori infection), dietary, as well as genetic factors [3] . H. pylori is considered as a definite carcinogen by the International Agency for Research on Cancer, and intestinal metaplasia has been suggested as the intermediate event in the development of H. pylori-related gastric cancer [4] . However, the molecular mechanism of this event needs to be further elucidated. In this issue of AMOR, a report from Ukraine's Vinnitsa National Pigorov Memorial Medical University by Sergii Vernygorodskyi attempts to improve our current understanding of the molecular mechanism associated with H. pylori-related gastric carcinogenesis [5] . The investigator found that the activation of CDX2, along with the simultaneous inactivation and a decreased number of genes (e.g., SHH, SOX2, and RUNX3) responsible for gastric differentiation, is a probable cause that leads to the appearance of intestinal metaplasia.Therefore, this study serves as an important catalyst to promote further research on the molecular mechanism and programming of gastric cancer cells, in hopes of gaining new knowledge in the prevention and treatment of gastric cancer. Conflict of interestThe author declares no potential conflict of interest with respect to the research, authorship, and/or publication of this article. References 1.Jemal scientist recounted the story of his dangerous experiment that led to him being awarded a Nobel Prize in 2005: "I had a patient with gastritis. I got the bacteria from his stomach and cultured them...I swizzled the organisms around in a cloudy broth and drank it the next morning."He added, "My stomach gurgled, and after five days...I'd run in the bathroom and vomit. After 10 days I had an endoscopy that showed the bacteria were everywhere. There was all this inflammation, and gastritis had developed."The Australian physician Dr. Barry Marshall, dubbed "the guinea-pig doctor" after the exploit, drank the germs as a last resort in his attempt to prove that the Helicobacter pylori (or "H. pylori") bacteria caused stomach ulcers, which could lead to cancer if left untreated.Ulcer's cure is relatively simple -antibiotics -but Dr. Marshall asserted that during his days as a physician, a majority of the medical elites believed that ulcers were caused by stress and dismissed unexplained conditions as "all in the head".As he was unable conduct his study on mice (H. pylori only affects primates), he ran the experiment on the only human patient who would consent to such a procedure: himself.More than a decade after the brave doctor infected himself and remedied his self-induced illness with ant...