Helicobacter pylori infection and carcinogenesis of the stomach.

摘要: Introduction: Human stomach carcinogenesis occurs after a multi-step process of genetic and epigenetic alterations in oncogenes, tumor-suppressor genes, cell-adhesion molecules, telomere telomerase activity as well instability at several microsatellite loci. Results discussion: These sequential found gastric cancer differ between the two histological types, indicating that different pathways exist for well-differentiated or intestinal-type poorly differentiated diffuse-type cancers, even though both types may arise from epithelial ”stem cells”, which express human reverse transcriptase (hTERT) protein activity. Infection with Helicobacter pylori, evidently causes release reactive oxygen species (ROMs) nitrogen (NO), be strong trigger cell” hyperplasia intestinal metaplasia, followed by reduction increased hTERT overexpression. They precede DNA replication error, hypermethylation, CD44 abnormal transcript, p53 mutations, all occur least 30% metaplasias early events pathogenesis type cancer. Here, we propose new concept preneoplasic lesion, ”metaplastic dysplasia”, based on our molecular observations.