Gastric ulcer patients are more susceptible to developing gastric cancer compared with concomitant gastric and duodenal ulcer patients.

Intestinal metaplasia (IM) and dysplasia are precancerous lesions of gastric cancer (GC); however, the prevalence of IM and dysplasia in patients exhibiting single gastric ulcer (GU) and concomitant gastric and duodenal ulcer (CGDU) varies. In the present study consecutive patients who had undergone esophagogastroduodenal endoscopy were retrospectively screened, and those presenting with GU or CGDU were further evaluated for IM and dysplasia. Patients diagnosed with GC or lymphoma and patients with a history of anti-Helicobacter pylori, non-steroidal anti-inflammatory medicine (NSAIM), H2-receptor antagonist or proton pump inhibitor therapy, were excluded from the present study. Of the 204,073 consecutively screened cases, 8,855 (4.3%) and 2,397 (1.2%) were diagnosed with GU and CGDU, respectively. A total of 1,722 GU and 233 CGDU patients were excluded; thus, 7,133 and 2,164 cases of GU and CGDU, respectively (n=9,297), were included in the present study. IM and dysplasia were observed in 1,348 (14.5%) and 210 (2.3%) patients, respectively. IM was more frequently identified in GU patients compared with CGDU patients (16.4 vs. 8.3%; odds ratio [OR], 2.158; 95% confidence interval [CI], 1.830-2.545; χ2=86.932; P<0.001); furthermore, GU patients exhibited significantly more frequent IM compared with CGDU patients at the gastric antrum (14.2 vs. 5.5%; OR, 2.818; 95% CI, 2.199-3.610; χ2=72.299; P<0.001), gastric incisura (24.0 vs. 14.1%; OR, 1.922; 95% CI, 1.502-2.432; χ2=30.402; P<0.001) and gastric corpus (12.6 vs. 3.3%; OR, 4.259; 95% CI, 1.030-17.609; χ2=4.736; P=0.026). Dysplasia was significantly more frequently identified in GU patients compared with CGDU patients (2.7 vs. 0.7%; OR, 4.027; 95% CI, 2.376-6.823; χ2=31.315; P<0.001), with GU patients exhibiting significantly more severe dysplasia at the gastric antrum (2.4 vs. 0.7%; OR, 3.339; 95% CI, 1.735-6.425; χ2=14.652; P<0.001) and the gastric incisura (2.9 vs. 0.7%; OR, 4.255; 95% CI, 1.694-10.689; χ2=11.229; P<0.001). Additionally, mild IM was more frequently identified in GU patients compared with CGDU patients (15.2 vs. 7.1%; OR, 2.353; 95% CI, 1.972-2.807; χ2=94.798; P<0.001) and dysplasia of a mild (1.7 vs. 0.6%; OR, 2.807; 95% CI, 1.580-4.987; χ2=13.519; P<0.001) or moderate/severe grade (1.1 vs. 0.09%; OR, 11.642; 95% CI, 2.857-47.439; χ2=18.896; P<0.001) was more frequent in GU patients compared with CGDU patients. IM and dysplasia were more frequently observed in GU compared with CGDU patients in the present study, which may be associated with an increased probability of developing GC.

[Establishment of a stable nasopharyngeal carcinoma cell line with lentivirus-mediated RNA interference for EIF4G1 gene silencing].

OBJECTIVE: To establish a nasopharyngeal carcinoma (NPC) cell line with stable EIF4G1 gene silencing induced by small interfering RNA (siRNA). METHODS: The EIF4G1 mRNA levels in 8 NPC cell lines including 5-8F, 6-10B, C666-1, CNE1, CNE2, HNE1, HONE1, and SUNE1 were detected by fluorescence quantitative RT-PCR (QRT-PCR). The recombinant lentivirus shRNA expression plasmid targeting EIF4G1 gene was packaged into mature lentivirus by 293FT cells and used to infect 5-8F cells. After blasticidin selection of NPC cells with constant expression of the EIF4G1-siRNA, the efficiency of EIF4G1 mRNA expression interference was determined using QRT-PCR. RESULTS: The 8 NPC cell lines showed differential expression of EIF4G1 mRNA, among which 5-8F cells had the highest EIF4G1 expression. The recombinant lentivirus plasmid pLenti6/BLOCK-iT-DEST/EIF4G1-shRNA was successfully constructed and verified by PCR and sequencing. The EIF4G1 mRNA level of 5-8F cells infected with shRNA-EIF4G1 lentivirus was significantly reduced as compared with the negative control and the blank control cells. CONCLUSION: The recombinant lentivirus vector pLenti6/BLOCK- iT-DEST/EIF4G1-shRNA we constructed results in marked downregulation of EIF4G1 mRNA expression and constant expression of EIF4G1-siRNA after infection of 5-8F cells.