• Journal of Preventive Medicine and Public Health
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• v.31 no.1 s.60
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• pp.91-103
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• 1998

Under experimental conditions, UVB radiation, a type of ultra violet radiation, has shown to .elate with the occurrence of skin erythema (sun-burn) in human and skin cancer in experimental animal. Cumulative exposure to UVB is also believed to be at least partly responsible for the 'aging' process of the skin in human. It has also been observed to have an effect of altering DNA (deoxyribonucleic acid). UVB radiation is both an initiator and a promoter of non-melanoma skin cancer. Meta-analysis is a new discipline that critically reviews and statistically combines the results of previous researches. A recent review of meta-analysis in the field of public health emphasized its growing importance. Using a meta-analysis in this study, we explored more reliable dose-response relationships between UVB radiation and skin cancer incidence. We estimated skin cancer incidence using measured UVB radiation dose at a local area of Seoul (Shin chou-dong). The studies showing the dose-response relationships between UVB radiation and non-melanoma skin cancer incidence were searched and selected for a meta-analysis. The data for 7 reported epidemiological studies of three counties (USA, England, Australia) were pooled to estimated the risk. We estimated rate of incidence change of skin cancer using pooled data by meta-analysis method, and exponential and power models. Using either model, the regression coefficients for UVB did not differ significantly by gender and age. In each analysis of variance, non-melanoma skin cancer incidence after removing the gender and age and UVB effects was significant (p>0.01). The coefficients for UVB dose were estimated $2.07\times10^{-6}$ by the exponential model and 2.49 by the power model. At a local area of Seoul (Shinchon-Dong), BAF value were estimated 1.90 and 2.51 by the exponential and power model, respectively. The estimated BAP value were increased statistical power than that of primary studies that using a meta-analysis method.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.11
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• pp.6721-6726
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• 2013

Background: Changes in DNA methylation patterns are believed to be early events in hepatocarcinogenesis. A better understanding of methylation states and how they correlate with disease progression will aid in finding potential strategies for early detection of HCC. The aim of our study was to analyze the methylation frequency of tumor suppressor genes, P14, P15, and P73, and a mismatch repair gene (O6MGMT) in HCV related chronic liver disease and HCC to identify candidate epigenetic biomarkers for HCC prediction. Materials and Methods: 516 Egyptian patients with HCV-related liver disease were recruited from Kasr Alaini multidisciplinary HCC clinic from April 2010 to January 2012. Subjects were divided into 4 different clinically defined groups - HCC group (n=208), liver cirrhosis group (n=108), chronic hepatitis C group (n=100), and control group (n=100) - to analyze the methylation status of the target genes in patient plasma using EpiTect Methyl qPCR Array technology. Methylation was considered to be hypermethylated if >10% and/or intermediately methylated if >60%. Results: In our series, a significant difference in the hypermethylation status of all studied genes was noted within the different stages of chronic liver disease and ultimately HCC. Hypermethylation of the P14 gene was detected in 100/208 (48.1%), 52/108 (48.1%), 16/100 (16%) and 8/100 (8%) among HCC, liver cirrhosis, chronic hepatitis and control groups, respectively, with a statistically significant difference between the studied groups (p-value 0.008). We also detected P15 hypermethylation in 92/208 (44.2%), 36/108 (33.3%), 20/100 (20%) and 4/100 (4%), respectively (p-value 0.006). In addition, hypermethylation of P73 was detected in 136/208 (65.4%), 72/108 (66.7%), 32/100 (32%) and 4/100 (4%) (p-value <0.001). Also, we detected O6MGMT hypermethylation in 84/208 (40.4%), 60/108 (55.3%), 20/100 (20%) and 4/100 (4%), respectively (p value <0.001. Conclusions: The epigenetic changes observed in this study indicate that HCC tumors exhibit specific DNA methylation signatures with potential clinical applications in diagnosis and prognosis. In addition, methylation frequency could be used to monitor whether a patient with chronic hepatitis C is likely to progress to liver cirrhosis or even HCC. We can conclude that methylation processes are not just early events in hepatocarcinogenesis but accumulate with progression to cancer.