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JPMPH : Journal of Preventive Medicine and Public Health

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3 "Mutation"
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Original Articles
Hepatitis B Virus DNA Mutation, Pattern of Major Histocompatibility Class-I among Familial Clustered HBV Carriers in Relation to Disease Progression .
Seung Pil Jung, Hyo Suk Lee, Chung Yong Kim, Yoon Ok Ahn
Korean J Prev Med. 2000;33(3):323-333.
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OBJECTIVES
Chronic HBsAg carriers are the principal source of infection for other susceptible people, and are themselves at high risk of developing serious liver diseases. In Korea, it has been estimated that 65-75% of the HBsAg positives remained as persistent carriers. Additionally, familial clustering of HBV infection has frequently been observed among carriers. Some would become progressive, chronic hepatitis patients, and others would not. The aim of this study was to evaluate the association between various factors, such as the duration of infection, type of virus, mutation of precore/core region in HBV, major histocompatibility class-I, and developing chronic liver diseases among familial HBV carriers. METHODS: Chronic carrier status was identified by repeated serological tests for HBsAg at intervals of six months or more. A familial chronic carrier was defined when the disease was observed in a family member over two generations. Two families were recruited, among which a total of 20 chronic HBsAg carriers(11 carriers in No.1, and 9 in No.2 family) were identified. Data on the general characteristics and liver disease status were collected. Identification of the HBV-DNA was successful only for 13 subjects among the 20 carriers. Analysis of viral DNA in terms of subtype, pre-core and core region mutations was carried out. The type of major histocompatibility class-I for the 13 subjects was also analysed. RESULTS & CONCLUSIONS: Seven of 10 chronic HBV carriers of the 1st generation and one of 10 of the 2nd generation were clinical patients with chronic hepatitis, the others, three of the 1st and nine of the 2nd generation, were asymptomatic carriers. This data indicates that the duration of HBV carriage is one of the major factors for disease severity. The subtype of HBsAg analysed using HBV-DNA identified in 13 carriers were adr, and the pattern of precore nonsense mutation in HBV-DNA was identical among family members, which means that the same virus strains were transmitted between the family members. The association between the precore or core mutations in HBV-DNA and the disease severity was not observed. While it was suggested that a specific type of MHC class-I may be related to disease progression.
Summary
Assessment of the Glycophorin A Mutant Assay as a Biologic Marker for Low Dose Radiation Exposure.
Mina Ha, Keun Young Yoo, Sung Whan Ha, Dong Hyun Kim, Soo Hun Cho
Korean J Prev Med. 2000;33(2):165-173.
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AbstractAbstract PDF
OBJECTIVES
To assess the availability of the glycophorin A (GPA) assay to detect the biological effect of ionizing radiation in workers exposed to low-doses of radiation. METHODS: Information on confounding factors, such as age and cigarette smoking was obtained on 144 nuclear power plant workers and 32 hospital workers, by a self-administered questionnaire. Information on physical exposure levels was obtained from the registries of radiation exposure monitoring and control at each facility. The GPA mutant assay was performed using the BR6 method with modification by using a FACScan flow cytometer. RESULTS: As confounders, age and cigarette smoking habits showed increasing trends with GPA variants, but these were of no statistical significance. Hospital workers showed a higher frequency of the GPA variant than nuclear power plant workers in terms of the NO variant. Significant dose-response relationships were obtained from in simple and multiple linear regression models. The slope of the regression equation for nuclear power plant workers was much smaller than that of hospital workers. These findings suggest that there may be apparent dose-rate effects. CONCLUSION: In population exposed to chronic low-dose radiation, the GPA assay has a potential to be used as an effective biologic marker for assessing the bone marrow cumulative exposure dose.
Summary
A Case-control Study for Assessment of Risk Factors of Breast Cancer by the p53 Mutation .
Heon Kim, Se Hyun Ahn, Moo Song Lee
Korean J Prev Med. 1998;31(1):15-26.
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AbstractAbstract PDF
p53 is the most frequently mutated gene in female breast cancer tissues and the prognosis of breast cancer could be changed by mutation of the gene. This study was performed to examine risk factors for breast cancer subtypes classified by p53 mutation and to investigate the roles of p53 gene mutation in carcinogenesis of breast cancer. The study subjects were 81 breast cancer patients and 121 controls who were matched to cases 1:1 or 1:2 by age, residence, education level and menopausal status. All the subjects were interviewed by a well-trained nurse with standardized questionnaire on reproductive factors, and were asked to fill the self-administrative food frequency and 24 hour recall questionnaires. p53 gene mutation in the cancer tissue was screened using polymerase chain reaction (PCR)-single strand conformational polymorphism (SSCP) method. Mutation type was identified by direct sequencing of the exon of which mobility shift was observed in SSCP analysis. Mutations were detected in p53 gene of 25 breast cancer tissues. By direct sequencing, base substitutions were found in 20 cancer tissues (10 transition and 10 transversion), and frame shift mutations in 5 (4 insertions and 1 deletion). For the whole cases and controls, risk of breast cancer incidence decreased when the parity increased, and increased when intake amount of total calory, fat, or protein increased. Fat and protein were statistically significant risk factors for breast cancer with p53 mutation. For breast cancer without p53 mutation, protein intake was the only significant dietary factor. These results suggests that causes of p53 positive breast cancer would be different from those of p53 negative cancer, and that dietary factors or related hormonal factors induce mutation of p53, which may be the first step of breast cancer development or a promoter following some unidentified genetic mutations.
Summary

JPMPH : Journal of Preventive Medicine and Public Health