10.22376/ijpbs.2019.10.1.p1-12 Volume 8 Issue 1 2017 (January - March) Four Histo-examination patterns of gastric biopsies used to study methylation status of lessThan i greaterThan p16 lessThan /i greaterThan promoter upon lessThan i greaterThan Helicobacter lessThan /i greaterThan lessThan i greaterThan pylori lessThan /i greaterThan infections. The incidence of lessThan i greaterThan H. pylori lessThan /i greaterThan in 120 samples was done by 23S ribosomal RNA gene. Statistical significant association (p= 0.03) have been showed between lessThan i greaterThan H. pylori lessThan /i greaterThan and carcinogenesis progression, comprising normal gastritis, atrophic gastritis, intestinal metaplasia and gastric cancer. Methyl-specific PCR showed that the methylation status of p16 promoter was increase during carcinogenesis progression (p=0.0015). Among 56 lessThan i greaterThan H. pylori lessThan /i greaterThan infected cases, 34(60%) were p16 promoter methylated. Within each disease step all lessThan i greaterThan H. pylori lessThan /i greaterThan infected cases showed higher p16 promoter methylation frequencies than lessThan i greaterThan H. pylori lessThan /i greaterThan non-infected cases, with increase status of methylation during disease progression. It was 33.3% in normal gastritis cases and raised 82.3% in cancer cases. The highly association between lessThan i greaterThan H. pylori lessThan /i greaterThan infection and hypermethylation of p16 promoter (p= 0.0009) confirms the role of lessThan i greaterThan H. pylori lessThan /i greaterThan in silencing of p16 gene. MOHAMMED FAWZI, ZAHRA M. AL-KHAFAJI SABAH N. AL-THAMIR Helicobacter pylori, P16, DNA methylation, tumor suppressor gene carcinogenesis 603-609