Mortality analysis of primary liver cancer in the mainland of China from 2004 to 2018 / 上海预防医学

Objective:To determine the mortality and changing trend of primary liver cancer by using the death data of Chinese mainland from 2004 to 2018. Methods:The death certificate data was collected from China National Mortality Surveillance System from 2004 to 2018. The crude mortality rate（CMR）and age-standardized mortality rate（ASMR）of primary liver cancer in different ages， regions and living environments were calculated by Joinpoint regression model to analyze the basic situation and mortality trend. Results:From 2004 to 2018， there were 556 241 primary liver cancer deaths in China， with a CMR of 25.18/105 and an ASMR of 17.98/105. It suggested that the mortality of primary liver cancer was on a decreasing trend. During the 15 years， the ASMR of primary liver cancer was 15.56/105 in urban areas and 19.29/105 in rural areas. In urban areas， CMR was 32.89/105 in males and 12.14/105 in females， respectively； while in rural areas， CMR was 38.39/105 in males and 14.02/105 in females， respectively. The CMR in eastern， central and western urban regions was 22.25/105， 22.66/105 and 23.50/105， respectively. The CMR in the rural areas of these three regions was 27.82/105， 26.98/105 and 23.85/105， respectively. The patients were divided into four age groups： 0-19 years old， 20-39 years old， 40-59 years old， and more than 60 years old. The CMR of four groups in urban areas was 0.14/105， 2.59/105， 24.51/105 and 91.80/105. In rural areas， the CMR of four groups was 0.17/105， 4.05/105， 32.16/105 and 103.02/105. Conclusion:From 2004 to 2018， the mortality rate of liver cancer in China has a decreasing trend. However， the primary liver cancer death burden is still serious because of the large population base， severe aging population problem， and significant urban-rural and male-female disparities in China.

Study on the relationship between single-nucleotide polymorphisms in IL-6, IL-10 genes and HBV-related hepatocellular carcinoma / 中华流行病学杂志

Objective To investigate the association between single nucleotide polymorphisms (SNPs)in cytokine IL-6, IL- 10 genes and HBV-related hepatocellular carcinoma(HCC). Methods A hospital-based case-control study was conducted in 381 cases with HBV-related HCC, 340 HBsAg carriers and 359 non-tumor controls. Genotypes of-572 site of IL-6 gene and-819, -592 sites of IL-10 gene were determined by real-time polymorphism chain reaction. Unconditional logistic regression was used to estimate the odds ratios(ORs)and 95 confidence intervals(C/s). Results For the G/C alleles of -572 loci on IL-6 gene, there were significant differences between the three groups(P＜0.05). Compared with CC genotype, GG genotype increased the risk of HBV infection (OR=2.171,95% Ch 1.068-4.415), but did not seem to be associated with HCC. For the alleles of-819 and -592 site of IL-10 gene, there were significant differences between the three groups(P＜0.05). Compared with CC genotype, TT genotype increased the risks of both HCC(OR=2.791,95%CI:1.326-5.874), and HCC in HBsAg carriers(0R=3.522,95%CI: 1.707-7.266). When compared with CC genotype on -592 site, the AA genotype reduced the risk of both HCC(OR=0.389, 95% CI:0.173-0.875), and HCC in HBsAg carriers(OR=0.336, 95% CI: 0.154-0.734). Conclusion The SNPs in -572 site of IL-6 gone might be associated with the risk of HBV infection. The SNPs in -819 site of IL-10 gene increased the risk of HCC, but -592 site of IL-10 gene decreased the risk of HCC.

Association of XPC and XPG polymorphisms with the risk of hepatocellular carcinoma / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To investigate whether the polymorphism of DNA repair genes XPC (Ala499Val and Lys939Gln) and XPG (His1104Asp) is associated with the susceptibility to hepatocellular carcinoma (HCC).</p><p><b>METHODS</b>A hospital-based case-control study was conducted in 500 cases with HCC and 507 controls. Genotypes of XPC and XPG were determined by real-time polymerase chain reaction with the TaqMan MGB probe.</p><p><b>RESULTS</b>Compared to the CC genotype, the CT genotype and the TT genotype of XPC Ala499Val were not associated with the susceptibility to HCC (adjusted OR = 1.34, 95% CI: 0.85-2.12; adjusted OR = 1.30, 95% CI: 0.68-2.51, respectively). Compared to the AA genotype, the AC genotype and the CC genotype of Lys939Gln were not associated with the susceptibility to HCC (adjusted OR = 1.20, 95% CI: 0.78-1.85; adjusted OR = 1.81, 95% CI: 0.88-3.73, respectively). Compared to the CC genotype, the CG genotype and the GG genotype of XPG His1104Asp were not associated with the susceptibility to HCC (adjusted OR = 0.85, 95% CI: 0.56-1.27; adjusted OR = 1.12, 95% CI: 0.67-1.87, respectively) However, the stratified analysis revealed that the females with the AC+CC genotype of XPC Lys939Gln had increased risk of HCC compared to those with AA genotype (OR = 2.17, 95% CI: 1.01-4.64).</p><p><b>CONCLUSION</b>Our results suggest that XPC and XPG polymorphisms do not independently affect on the susceptibility to HCC, but the joint effect of C allele of XPC Lys939Gln and female may modify the risk of HCC.</p>

Study on the relationship between hepatocellular carcinoma and the interaction between polymorphisms in DNA repair gene XPD and environmental factors / 中华流行病学杂志

Objective To study the relationship between hepatocellular carcinoma and the interaction of polymorphisms in DNA repair gene XPD with environmental factors. Methods A hospital-based ease-control study on hepatoeellular carcinoma was conducted. All the hepatocellular carcinoma eases (n=300) were newly diagnosed and controls (n=312) were diagnosed with non-tumor cases. XPD genotype (Lys751 Gin and Asp312 Ash) from blood derived DNA was determined using TaqMan MGB Real-time PCR. Unconditional logistic regression was used to estimate the odds ratios (ORs) and 95% confidence intervals (CIs). Results For XPD condon 751 genotypes, there was no significant difference between frequencies of the AC or CC among patients and controls (P>0.05) (referent AA). The frequency of XPD312A allelic gene was higher in eases than that in controls and was associated with an increased risk (adjusted OR = 2.62,95% CI: 1.626-4.222) for hepatocellular carcinoma when compared with GG genotype. Interactions were found between infection of HBsAg and XPD312 (OR=7.348), as well as between smoking and non-wild type gene of XPD751 (0R=4.291) and XPD312 (OR=5.341). Conclusion DNA repair XPD312A allelic gene might increase the risk of Hepatocellular carcinoma. Interactions between HBsAg infection, smoking and XPD were observed in Hepatocellular carcinoma.

Synergistic effect of HBV infection, alcohol and raw fish consumption on oncogenisis of primary hepatic carcinoma / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To study the correlation of eating raw fish with primary hepatic carcinoma (PHC), and to investigate the synergistic effect of HBV infection, alcohol consumption and eating raw fish on the oncogenesis of PHC.</p><p><b>METHODS</b>A hospital-based case-control study was conducted among 500 PHC patients and 500 non-cancerous patients in order to compare the history of eating raw fish. The synergistic pathogenetic action of eating raw fish, HBV infection and alcohol consumption on carcinogenesis of PHC was analyzed by crossover analysis and multiple logistic regression.</p><p><b>RESULTS</b>The rates of eating raw fish in the past between the case (54.8%) and the control group (8.4%) were significantly different (P < 0.001). OR value of suffering PHC in the patients who ate raw fish in the past was 13.6 (95% CI: 9.1-19.5) when compared with the non-cancerous patient. HBV infection, alcohol consumption and eating raw fish showed an interactive effect on the development of PHC, with a relative excessive risk of interaction(RERI) of 195.3 and 17.8; attributable proportion of interaction (API) of 0.8630 and 0.5251; and synergy index (S) of 7.5 and 2.8, respectively.</p><p><b>CONCLUSION</b>A history of eating raw fish may be an important risk factor for suffering primary hepatic carcinoma. HBV infection, alcohol consumption and eating raw fish may have a synergistic effect on the developing of primary hepatic carcinoma.</p>

Etiologic fraction and interaction of risk factors for primary hepatic carcinoma in Guangxi, China / 中华预防医学杂志

<p><b>OBJECTIVE</b>To explore etiologic fraction (EF) and interaction of hepatitis B virus (HBV) infection and other risk factors for primary hepatocellular carcinoma (PHC) in Guangxi, China.</p><p><b>METHODS</b>A hospital-based case-control study including 500 PHC patients and 500 nontumorous patients was carried out in Guangxi. EF and interactions of HBV infection and other risk factors for PHC were analyzed by crossover analysis and nonconditional multiple logistic regression.</p><p><b>RESULTS</b>HBV infection, family history of PHC, diabetes mellitus, eating raw fish, heavy alcohol consumption, frequently used drug, low income, mental oppression and blood type B all were risk factors for PHC. With EFs of 0.725, 0.186, 0.119, 0.486, 0.385, 0.438, 0.277, 0.607, 0.299, respectively and with etiologic fractions attributable to interaction [EF(A xB)] of 0.736, 0.643, 0.849, 0.551, 0.592, 0.618, 0.902, 0.577; and indices of interaction of 0.743, 0.651, 0.853, 0.560, 0.600, 0.626, 0.907, 0.586, respectively.</p><p><b>CONCLUSION</b>Main risk factors for PHC might include HBV infection, family history of PHC, diabetes mellitus, eating raw fish, heavy alcohol consumption, frequently used drug, low income, mental oppression and blood type B. HBV infection with other risk factors might exert synergistic action on developing PHC and increase the risk of PHC.</p>

Evaluation of the risk of clonorchiasis inducing primary hepatocellular carcinoma / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To explore the relationship between clonorchiasis and primary hepatocellular carcinoma (HCC) and analyze the synergistic actions of HBV infection, alcohol consumption and clonorchiasis on HCC development.</p><p><b>METHODS</b>This hospital-based case-control study was conducted among 444 HCC patients (cases) and 500 non tumor patients (controls) to compare the prevalence of clonorchiasis in the cases and the controls. The risk of clonorchiasis and the synergistic actions between HBV infection, alcohol consumption and clonorchiasis on HCC development were analyzed by crossover analysis and multiple logistic regression.</p><p><b>RESULTS</b>The prevalence of clonorchiasis in the cases (16.44%) was much higher than that of the controls (2.40%) (X2 = 56.58, P less than 0.01). In the case group, the OR value of those with clonorchiasis was 8.00 (95% CI: 4.34-14.92). The OR value was 4.82 (95% CI: 2.32-10.26) for the subjects whose clonorchiasis was diagnosed less than 10 years before their diagnosis of HCC, and was 17.54 (95% CI: 5.47-57.18) for those whose HCC was diagnosed more than 10 years ago. HBV infection, alcohol consumption and clonorchiasis showed an additive interaction in the development of HCC, with a relative excess risk of interaction of 110.43 and 18.23; attributable proportion of interaction of 0.80 and 0.63; synergy index of 5.18 and 2.84, respectively.</p><p><b>CONCLUSION</b>Clonorchiasis could be an important risk factor for HCC. When the course of clonorchiasis is prolonged, the risk of HCC could increase. HBV infection, alcohol consumption and clonorchiasis might have synergistic actions on the development of HCC.</p>

Expression of cyclooxygenase-2 in esophageal squamous cell carcinogenesis / 中华预防医学杂志

<p><b>OBJECTIVES</b>To investigate the expression of cyclooxygenase-2 (cox-2) protein in normal squamous epithelium, squamous dysplasia and squamous cell carcinoma of the esophagus, and to elucidate the role of cox-2 in esophageal carcinogenesis.</p><p><b>METHODS</b>Biopsy specimens of atypical esophageal dysplasia (n = 47) and surgical resection of squamous cell carcinoma (n = 86) were compared with normal esophageal specimens (n = 42) and the expression of cox-2 in those specimens was analyzed by immunohistochemistry and western blotting.</p><p><b>RESULTS</b>A significant elevated cox-2 expression was shown in atypical esophageal squamous dysplasia and squamous cell carcinoma, as compared to that in normal esophageal squamous epithelium, with immunohistochemical stain scores of 2.67 +/- 1.77, 2.19 +/- 1.79 and 0.71 +/- 0.46, respectively. Results of western blotting analysis confirmed those obtained by immunohistochemistry. Cox-2 expression significantly correlated with proliferation activity assessed by proliferating cell nuclear antigen index in dysplastic and carcinomous lesions, respectively, and no such correlation could be found in normal esophageal mucosa. Elevated cox-2 expression was not associated with clinical-pathological features of esophageal squamous carcinoma, including age, gender, tumor size, histological grade, lymph node metastasis and clinical stage.</p><p><b>CONCLUSION</b>Elevated expression of cox-2 in atypical squamous dysplasia and squamous cell carcinoma of the esophagus, which correlated with cell proliferation activity, indicated that cox-2 may be involved in the early stage of squamous carcinogenesis of the esophagus, and may be a target of prevention and treatment for esophageal squamous cell carcinoma.</p>

Significance of p53 gene mutation and P53 protein expression abnormality on the prognosis of esophageal cancer: a meta-analysis study / 中华流行病学杂志

<p><b>OBJECTIVE</b>To evaluate the prognostic significance of p53 mutation and P53 protein expression abnormality among esophageal cancer.</p><p><b>METHODS</b>The results of 27 random controlled trials from 1990 to 2003 were analyzed by meta-analysis method. The overall positive rate of p53 was 52.9% among the cumulative 2174 cases. Relative hazard (RH) was applied to evaluate the risk of disease and all data were analyzed by Dersimonian-Laird method.</p><p><b>RESULTS</b>The analysis for homogeneity (q statistics test) showed that all eligible studies were with heterogeneity (q = 59.88, P < 0.005). The combined RH was 2.07 and 95% confidence interval was 1.58-2.70.</p><p><b>CONCLUSION</b>Findings showed that p53 was a poor prognosis biomarker for esophageal cancer gene diagnosis but might benefit to the strategy of treatment.</p>

Expression of telomerase reverse transcriptase in premalignant esophageal squamous dysplasia / 中华流行病学杂志

<p><b>OBJECTIVE</b>To study the relationship of human telomerase reverse transcriptase (hTRT) and malignant transformation of esophageal dysplasia.</p><p><b>METHODS</b>Telomerase activity and hTRT expression in esophageal dysplasia (n = 47), squamous cell carcinoma (n = 29) and normal esophagus (n = 11) were detected by telomeric repeat amplification protocol (TRAP) and in situ hybridization, respectively.</p><p><b>RESULTS</b>Telomerase activity was detected in none of the 11 cases of normal esophageal tissues (0%) but in 21 of 47 cases (44.7%) of dysplasia, and in 25 of 29 cases (86.2%) of esophageal squamous cell carcinoma. There were statistically significant differences among the telomerase activity in normal esophagus, esophageal dysplasia, and in squamous cell carcinoma (chi(2) = 5.89, P < 0.05; chi(2) = 11.35, P < 0.01). hTRT mRNA was expressed in none of the 11 cases of normal esophageal tissues (0%) but in 23 of 47 cases (48.9%) of dysplasia, and in 24 of 29 cases (82.8%) of esophageal squamous cell carcinoma. There were statistically significant differences among the expression of hTRT mRNA in normal esophagus, esophageal dysplasia, and in squamous cell carcinoma (chi(2) = 6.99, P < 0.01; chi(2) = 7.32, P < 0.01). Significant correlation was found between the telomerase activity and the expression of hTRT mRNA (chi(2) = 57.91, P < 0.001).</p><p><b>CONCLUSION</b>The mRNA expression of hTRT which paralleled to telomerase activity implied that there was a crucial role to play in regulating the activation of telomerase, and was closely related to the malignant transformation of esophageal dysplasia. hTRT might serve as a new, valuable biomarker to detect esophageal squamous cell carcinoma.</p>