| Background:Gastric epithelial dysplasia is the most important precancerous lesions of gastriccancer and has the important clinical significance. There is universally recognizedthat Gastric cancer model: normal mucosa-chronic superficial gastritis-chronicatrophic gastritis-intestinal metaplasia-dysplasia-early gastric cancer-advancedgastric cancer, were proposed by Correa in1988.With the development of molecularbiology techniques, people gradually realize that many important changes lead toabnormal cell proliferation and differentiation at the molecular level, and even someclonal growth already occurred before the traditional light microscope to identifymorphological changes, cancer morphological changes is a relatively late event. Thispaper attempts to use objective and accurate biological markers associated with thediagnosis of dysplasia, and explore the significance of dysplasia diagnosis tocombine with these molecular markers, especially for moderate.Materials and Methods:Collected145cases gastric biopsy specimens from the Endoscopy CenterPathology, First Hospital of Jilin University, including gastric inflammation20cases,mild dysplasia20cases, moderate dysplasia47cases, severe dysplasia29cases,gastric adenocarcinoma29cases. The clinical features(gender, age, location) andmorphological characteristics of each group were analyzed, usingimmunohistochemical staining technique,widely accepted and researched moremature molecular biology markers:c-Met,CX43,CyclinD1,COX-2,P53and Ki67diagnostic of dysplasia. Score was calculated according percentage and stainingintensity of positive cells in the lesions expressed. Finally, the median value of eachgroup were calculated and comparison,six antibodies scores by adding the total score for each patient.Results:1. Clinical general comparison: the average age of stomach inflammationgroup:52.9; severe dysplasia and gastric adenocarcinoma:61.2and65.9, respectively,significantly higher than the inflammation group(P <0.05);while mild and moderate:56.3and59.1,respectively, compared with the inflammation group, the differencewas not statistically significant(P>0.05),there is no comparison between the twogroups was significant(P>0.05);gastric adenocarcinoma group were comparedwithmild, moderate dysplasia group, the difference was significant(P<0.05),comparedwith the severe dysplasia group, the difference was not significant(P>0.05).Male andfemale incidence ratio: incidence ratio of men and women in gastric inflammationgroup and mild dysplasia group fairly moderate dysplasia group, men more thanwomen in severe dysplasia and gastric adenocarcinoma; diseased parts: gastricinflammation group and gastric adenocarcinoma group no significant differences,gastric antrum was significantly more than gastric body in mild dysplasia, moderatedysplasia and severe dysplasia group.2.The positive expression rates of c-Met in gastric inflammation group were35%, and the adenocarcinoma group, severe dysplasia and moderate dysplasia groupwere96.6%,86.2%,76.6%, significantly higher than gastric inflammation group(P<0.001); mild dysplasia group were45%,compared with inflammation group, thedifference was not significant(P=0.51);while moderate dysplasia group, severedysplasia group and gastric adenocarcinoma group were no significant difference (P>0.01).3. The Expression of CX43in gastric inflammation group, mild dysplasia,moderate dysplasia, severe dysplasia and gastric adenocarcinoma group were75%ã€65%ã€61.7%ã€55.2%ã€48.3%, gradually decreased, the positive expression rate of CX43have no statistically significant difference in the overall five groups(P>0.01).4. CyclinD1and COX-2expression in gastric inflammation group, milddysplasia, moderate dysplasia, severe dysplasia and gastric adenocarcinoma group were65%ã€75%ã€78.7%ã€72.4%ã€82.8%and85%ã€90%ã€100%ã€96.6%ã€96.6%,graduallyincreased; positive expression rate have no significant difference in the overall fivegroups(P>0.01).5. There is almost no expression of P53in gastric inflammation group, positiveexpression rate of P53in moderate dysplasia, severe dysplasia and gastricadenocarcinoma group were74.5%,48.3%and72.4%; there were significantlyhigher than inflammation group(P<0.001).Expression ratio of P53in mild dysplasiawere5%, compared with moderate dysplasia, severe dysplasia and gastric cancergroup were significantly difference(P<0.001);P53expression were no differencesamong moderate dysplasia group, severe dysplasia and gastric adenocarcinomagroup (P>0.01).6. The positive expression rates of Ki67in gastric inflammation group were40%, and the adenocarcinoma group, severe dysplasia, moderate dysplasia group andmild dysplasia group ware almost all100%, significantly higher than gastricinflammation group (P<0.001); Ki67expression were no differences among milddysplasia, moderate dysplasia group, severe dysplasia and gastric adenocarcinomagroup (P>0.01).7. Respectively, expression score were statistically significant in the overallbetween the groups. Respectively, each cases of the six antibody staining scoresummed statistical analysis: gastric cancer median value was28points, severedysplasia median value was26points, moderate dysplasia median value was23points, mild dysplasia median value was16points.27.6%(8cases) cases of Severedysplasia group was greater than gastric cancer group;12.8%(6cases) cases ofmoderate dysplasia group was greater than gastric cancer group,12.8%(6cases) ofthe cases of severe dysplasia was greater than the median value;5%(1case)of milddysplasia group was greater than moderate dysplasia group.Conclusions:1.Expression of c-Met,CyclinD1,COX-2,P53,Ki67was increased and CX43was decreased may promote the occurrence of gastric cancer; 2.Composite score of c-Met,CX43,CyclinD1,COX-2,P53and Ki67,25.6%cases in moderate dysplasia will be required to clinical intervention;3.The c-Met, CX43, CyclinD1, COX-2, P53and Ki67expression in the sixantibodies in gastric epithelial dysplasia scores were statistically analyzed gastricepithelial dysplasiais expected to assist the diagnosis, assessment the high-risk casesof moderate dysplasia, and provide an objective theoretical basis for clinicaltreatment. |