{'fraction_non_alphanumeric': 0.013522650439486139, 'fraction_numerical': 0.000676132521974307, 'mean_word_length': 5.63677130044843, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Helicobacter pylori and Epigenetic Mechanisms Underlying Gastric Carcinogenesis

Gastric carcinogenesis is a multistep process triggered by Helicobacter pylori and characterized by accumulation of molecular alterations. Two mechanisms are implicated in cancer-related molecular alterations: genetic and epigenetic. The former includes changes in the DNA sequence, the latter occurs without changes of DNA sequence. However, the most important difference between genetic and epigenetic alterations is that epigenetic changes are potentially reversible by eliminating toxic agents. DNA methylation is the major epigenetic phenomenon of eukaryotic genomes and involves the addition of a methyl group to the carbon 5 position of the cytosine ring within the CpG dinucleotide. DNA methylation is needed for the normal development of cells, whereas aberrant methylation of CpG islands confers a selective growth advantage that results in cancerous growth. The stomach is one of the organs frequently showing aberrant methylation of DNA epithelial cells because of its accessibility to exogenous toxic agents such as H. pylori infection. Aberrant methylation of CpG islands occurs early in gastric carcinogenesis, tends to increase as the process advances and is prevalently related to the infection. In conclusion, gastric cancer is mainly an epigenetic disease and H. pylori, acting through inflammatory mediators, may play a key role in the development of such molecular alterations.