Search

Background and Aim: This study aimed to estimate the time to precursor progression and to identify significant predicators. Methods: One hundred thirty-three precursor and 311 normal cases detected in a population- based screening were surveyed for 5.5 years. Precursor progression was defined as worsening of dysplasia or development of a new precursor. Time to precursor progression was estimated by the Kaplan-Meier method. Significant predicators were estimated by Cox proportional regression. Results: Of the 133 precursor cases, 33.08% (44/133) progressed or recurred, 30.08% (40/ 133) persisted, and 36.84% (49/133) regressed; of the 311 normal subjects, 13.50% (42/ 311) developed a precursor. Progression occurred significantly earlier and more frequently with ncreasing histology: with mind dysplasia (mD), 7.8% progressed by 1 year and 23.3% progressed by 5 year; with moderate dysplasia (MD), 18% progressed by 1 year and 70% progressed by 5 years; and with severe dysplasia, 50% progressed by 1 year and 100% progressed by 5 years. The difference between any two groups was significant. In addition, the marginal Lugol-stained mucosa at endoscopic mucosal resection had a progressing risk similar to that of MD, and basal cell hyperplasia was similar to that of mD. Significant predicators for precursor progression included male sex (hazard ratio and 95% CI: 2.74 (1.63-4.60)), age over 50 years (2.31 (1.33-4.02)), family history of upper gastrointestinal cancer (UGIC) (1.56 (1.00-2.45)), multifocal dysplasia (5.11 (3.01-8.68)), and baseline histology. Conclusions: Sex, age, family history of UGIC, multifocal dysplasia, and baseline histology are significant independent predicators for precursor progression. Patients after endoscopic mucosal resection should be continuously surveyed. [ABSTRACT FROM AUTHOR]

Aims Esophageal cancer ( EC) is one of the most prevalent and deadly cancers worldwide. Along with nutrition, smoking and alcohol consumption, human papillomavirus ( HPV) infection is one of the major risk factors, which is modulated by host immune response. This study is aimed at elucidating how HPV modifies host immune system in the EC pathogenesis. Methods The HPV and HLA- DQB1 levels in primary esophageal squamous cell (ESC) cancer cells from Han, Khazak and Uygur patients were analyzed by quantitative real-time PCR and immunoblotting. The ability of HPV16 E6/E7 to transform normal primary ESCs was investigated by infecting ESC with pMSCVpuro-carried E6 or E7. The shRNA against HPV16 E6 or E7 was delivered by adenovirus into esophageal squamous cell carcinoma ( ESCC) cells with high HPV content. The DNA methylation level of HLA- DQB1 was measured by methylation-specific PCR. Results The HLA- DQB1 expression level was correlated with the levels of HPV and inversely related to DNA methylation level of HLA- DQB1. Overexpressing HPV16 E6 or E7 alone was enough to transform normal primary ESCs. However, single knockdown of either E6 or E7 in ESC cancer cells did not reduce HLA- DQB1 expression. Conclusions Oncogenic HPV E6 and E7 genes promoted ESCC pathogenesis by upregulating susceptible HLA- DQB1 via DNA demethylation. [ABSTRACT FROM AUTHOR]