[Estimated of esophageal cancer incidence and mortality in China, 2013].

Objective: The National Central Cancer Registry (NCCR) collected esophageal data of local cancer registries in 2013 to estimate the incidence and mortality in China. Methods: Data submitted from 347 registries were evaluated and 255 registries' data are qualified by NCCR. Data of incidence and mortality were stratified with areas (urban/rural), gender and age group. Chinese population census in 2000 and Segi's population were used for age-standardized incidence/mortality. Results: All of 255 cancer registries covered a total of 226 494 490 population (111 595 772 in urban areas and 114 898 718 in rural areas). The morphology verified cases (MV%) of esophageal cancer accounted for 75.51% and 1.64% of incident cases were identified through death certifications only (DCO%) with mortality to incidence ratio of 0.75. The estimates of new esophageal cancer cases and deaths were 277 thousand and 206 thousand in China, respectively. The crude incidence rate of esophageal cancer in Chinese cancer registration areas was 20.35/10(5) (28.15/10(5) in male, 12.15/10(5) in female), age-standardized incidence rates by Chinese standard population (ASIRC) and by world standard population were 13.64/10(5) and 13.82/10(5) with the cumulative incidence rate (0-74 age years old) of 1.77%. The esophageal cancer incidence and ASIRC were 13.38/10(5) and 8.74/10(5) in urban areas whereas in rural areas, they were 28.44/10(5) and 19.56/10(5,) respectively. In rural areas, the crude incidence rate of esophageal cancer was 2.13 times higher than that in urban areas, and after age-standardized it remained 2.24 times higher. The esophageal cancer mortality in Chinese cancer registration areas was 15.17/10(5) (20.86/10(5) in male and 9.20/10(5) in female), age-standardized mortality by Chinese standard population (ASMRC) and by world standard population were 9.95/10(5) and 9.98/10(5,) with the cumulative mortality rate (0-74 age years old) of 1.20%. The esophageal cancer mortality and ASMRC were 10.12/10(5) and 6.46/10(5) in urban areas, whereas in rural areas, they were 21.05/10(5) and 14.16/10(5,) respectively. In rural areas, the esophageal cancer mortality and ASMRC were 2.08 and 2.19 times higher than those in urban areas. Esophageal cancer was the sixth common cancer and the fourth leading causes of cancer death, accounting for about 7.52% of all cancer cases and 9.26% of all cancer deaths. Conclusions: Esophageal cancer is one of the most common cancers in China. Screening and early detection are important to reduce the incidence and mortality.

Association of CDH1 single nucleotide polymorphisms with susceptibility to esophageal squamous cell carcinomas and gastric cardia carcinomas.

E-cadherin (CDH1) is a tumor suppressor involved in epithelial cell-cell interactions. Single nucleotide polymorphisms (SNP) in the CDH1 gene, -160C/A and -347G/GA in the 5'-promoter region and +54C/T in the 3'-untranslated region (UTR) have been shown to be associated with tumor development and progression via modifying transcriptional activity, mRNA stability or protein expression. To investigate the influence of CDH1 SNP on susceptibility to esophageal squamous cell carcinomas (ESCC) and gastric cardia adenocarcinomas (GCA), a case-control study was conducted among 333 ESCC patients, 239 GCA patients and 343 controls from a northern Chinese population. CDH1 polymorphisms were genotyped by polymerase chain reaction-restriction fragment length polymorphism analysis. The results showed that; (i) genotypes with the +54C allele (C/C or C/T) significantly increased the risk of developing both ESCC and GCA compared to the +54T/T genotype (age and gender adjusted odds ratio [OR] = 1.45 and 2.28, 95% confidence interval [CI] = 1.06-1.99 and 1.58-3.30, respectively), and this association was significant only among non-smokers (OR = 1.68 and 2.64, 95% CI = 1.01-2.80 and 1.43-4.87 for ESCC and GCA, respectively), and individuals without a family history of upper gastrointestinal cancer (OR = 2.63 and 2.97, 95% CI = 1.36-5.10 and 95% CI = 1.32-6.68 for ESCC and GCA, respectively); (ii) compared with the -347G/G genotype, the -347GA and GA/GA genotypes significantly increased the risk of developing GCA (OR = 1.45, 95 % CI = 1.03-2.04); (iii) there was a significant association of CDH1-160C/-347G/+54C and -160C/-347GA/+54C haplotypes with the development of GCA, compared with the -160C/-347G/+54T haplotype (OR = 1.80 and 2.21, 95% CI = 1.33-2.44 and 1.43-3.42, respectively); and (iv) the influence of CDH1 SNP on the depth of tumor invasion and lymphatic metastasis in ESCC and GCA patients was not observed in this study. The present study indicates that CDH1 polymorphisms might modify susceptibility to ESCC and/or GCA.

PTEN polymorphisms and the risk of esophageal carcinoma and gastric cardiac carcinoma in a high incidence region of China.

PTEN, as a tumor suppressor gene, plays an important role in regulating cell growth, proliferation, and apoptosis. Two common polymorphisms, -9C/G and IVS4 (-/+), may alter susceptibility to the disease. To test the hypothesis that the genetic variations of PTEN play a role in the etiology of esophageal squamous cell carcinoma (ESCC) and gastric cardiac adenocarcinoma (GCA), a population-based case-control study was conducted in 350 ESCC patients, 257 GCA patients, and 634 healthy controls from a high-incidence region of Hebei province, China. The PTEN polymorphisms were genotyped by polymerase chain reaction-restriction fragment length polymorphism analysis (PCR-RFLP). The results showed that the family history of upper gastrointestinal cancer (UGIC) significantly increased the risk of developing ESCC and GCA (the age, gender and smoking status adjusted OR = 1.73 and 1.67; 95% CI = 1.29-2.32 and 1.28-2.19, respectively). The overall distribution of the PTEN -9C/G genotype was not significantly different between cancer patients and controls. Compared with the PTEN IVS4-/- genotype, the IVS4+/+ genotype significantly decreased the risk of ESCC and GCA development, the adjusted OR was 0.64 (95% CI = 0.44-0.94) and 0.63 (95% CI = 0.41-0.98), respectively. Stratification analysis by gender, age, smoking status and family history of UGIC showed that the PTEN IVS4-/+ genotype only reduced the risk of ESCC (adjusted OR = 0.55, 95%CI = 0.34-0.90) among subjects with family history of UGIC. While the IVS4+/+ genotype decreased the susceptibility to both ESCC and GCA (adjusted OR = 0.61 and 0.57, 95% CI = 0.37-0.98 and 0.34-0.98, respectively) among male subjects, the IVS4+/+ genotype only decreased the risk of ESCC development among subjects younger than 55 years (adjusted OR = 0.43, 95% CI = 0.21-0.85). In addition, the haplotype analysis found that the -9C/IVS4- haplotype increased the risk of developing ESCC and GCA (OR = 1.31 and 1.24, 95% CI = 1.08-1.58 and 1.001-1.53). Our results suggested that the PTEN IVS4+/+ homozygote may play a protective role in the development of ESCC and GCA, while the haplotype -9C/IVS4- might be the risk factor of the development of ESCC and GCA in the high incidence region population of Hebei province, China.

The p73 polymorphisms are not associated with susceptibility to esophageal squamous cell carcinoma in a high incidence region of China.

P73, a p53 homolog, has some p53-like activities and plays an important role in modulating cell cycle, apoptosis and DNA repair. The two linked polymorphisms in the non-coding region of exon2 of p73 gene, named G4C14-A4T14, may alter translation efficiency of the gene. The transcription of p73 gene is initiated by three promoters, termed P1-P3. There is a single nucleotide substitution (-386G/A) in the P3 promoter region with unknown function. To test the hypothesis that the genetic variations in the exon2 and P3 promoter play a role in the etiology of esophageal squamous cell carcinoma (ESCC), we conducted a population-based case-control study in 348 ESCC patients and 583 healthy controls from a high incidence region of Hebei province, China. The p73 polymorphisms were genotyped by polymerase chain reaction-restriction fragment length polymorphism analysis (PCR-RFLP). The results showed that the family history of upper gastrointestinal cancer (UGIC) significantly increased the risk of developing ESCC (the age, sex and smoking status adjusted OR = 2.02, 95% CI = 1.54-2.67). The overall distribution of the p73 genotype, allelotype and haplotype in cancer patients and controls were not significantly different (all P-values are above 0.05). Stratification analysis by smoking status and family history of UGIC also did not show the significant influence of the polymorphisms on the risk of ESCC development. The results suggested that the p73 exon2 G4C14-A4T14 and P3 promoter -386G/A polymorphisms might not be used as potential markers to predicate the risk of ESCC development in northern China.