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5. Comparison of Reading Results Between Experts and Beginners After a Brief Lecture on the International Classification of High-Resolution Computed Tomography for Occupational and Environmental Respiratory Diseases

Author

TAMURA, Taro, NAGOSHI, Kiwamu, SUBHANNACHART, Ponglada, DUMAVIBHAT, Narongpon, AKIRA, Masanori, SUZUKI, Kazuhiro, LYNCH, David A., HERING, Kurt G., VEHMAS, Tapio, HIRAKU, Yusuke, SUGANUMA, Narufumi, and KUSAKA, Yukinori

Subjects
training, pneumoconiosis, asbestosis, reading trial, ICOERD, HRCT
Abstract

This study compared interpretation of irregular and/ or linear opacities (IR) among experts and beginners who learned the International Classification of High-Resolution Computed Tomography for Occupational and Environmental Respiratory Diseases. The accuracy of interpretation of results among beginners was consistent compared to that of experts after training. It is important to further improve and develop training methods and materials for inexperienced physicians.

Published
2022

10. Combination of RERG and ZNF671 methylation rates in circulating cell‐free DNA: A novel biomarker for screening of nasopharyngeal carcinoma

Author

Xu, Yifei, primary, Zhao, Weilin, additional, Mo, Yingxi, additional, Ma, Ning, additional, Midorikawa, Kaoru, additional, Kobayashi, Hatasu, additional, Hiraku, Yusuke, additional, Oikawa, Shinji, additional, Zhang, Zhe, additional, Huang, Guangwu, additional, Takeuchi, Kazuhiko, additional, and Murata, Mariko, additional

Published
2020
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20. Oxidative DNA Damage and Apoptosis Induced by Aclarubicin, an Anthracycline: Role of Hydrogen Peroxide and Copper

Author

MIZUTANI, HIDEKI, primary, HAYASHI, YUKA, additional, HASHIMOTO, MIYABI, additional, IMAI, MASANORI, additional, ICHIMARU, YOSHIMI, additional, KITAMURA, YUKI, additional, IKEMURA, KENJI, additional, MIYAZAWA, DAISUKE, additional, OHTA, KINYA, additional, IKEDA, YOSHIAKI, additional, MAEDA, TOHRU, additional, YOSHIKAWA, MASAE, additional, HIRAKU, YUSUKE, additional, and KAWANISHI, SHOSUKE, additional

Published
2019
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36. 酸化ストレスによるクラスターDNA損傷機構とその変異における役割(日本環境変異原学会第32回大会シンポジウム2「DNA損傷と変異のメカニズム」)

Author

Oikawa, Shinji, Ohnishi, Shiho, Murata, Mariko, Hiraku, Yusuke, and Kawanishi, Shosuke

Subjects
reactive oxygen species, DNA damage, hotspot, double base lesions, carcinogenesis
Abstract

Reactive oxygen species generated by environmental factors, such as radiation, UV and chemicals can cause sequence-specific DNA damage and play important roles in mutagenesis and carcinogenesis. We have investigated sequence specificity of oxidative stress-mediated DNA damage by using ^P-labeled DNA fragments obtained from the human c-Ha-ras-1, p53 and p16 genes. Free hydroxyl radicals cause DNA damage with no marked site specificity. Copper-hydroperoxo complex caused DNA damage at thymine, cytosine and guanine residues. ^1O_2 preferentially induces lesions at guanine residues. Benzoyloxyl radical specifically causes damage to the 5'-G in GG sequence ; this sequence is easily oxidized because a large part of the highest occupied molecular orbital of this radical is distributed on this site. Recently, we demonstrated that BP-7, 8-dione, a metabolite of carcinogenic benzo [a] pyrene (BP), strongly damaged the G and C of the 5'-ACG-3' sequence complementary to codon 273 of the p53 gene in the presence of NADH and Cu (II). BP-7, 8-dione also caused preferential double base lesion at 5'-TG-3' sequences. Since clustered DNA damage is poorly repaired, it is speculated that induction of the double base lesions in DNA might lead to activation of proto-oncogene or inactivation of the tumor suppressor gene. Therefore, oxidative DNA damage induced by BP-7,8-dione, especially double base lesions, may participate in the expression of carcinogenicity of BP in addition to DNA adduct formation. Here, we discuss the mechanisms of sequence-specific DNA damage including clustered DNA damage in relation to mutagenesis and carcinogenesis.

Published
2004

37. 環境因子による酸化的DNA損傷とがん,老化 : 第12回公開シンポジウム : 活性酸素の分子病態学

Author

Oikawa, Shinji, Murata, Mariko, Hiraku, Yusuke, and Kawanishi, Shosuke

Subjects
reactive oxygen species, aging, DNA damage, carcinogenesis, environmental chemicals
Abstract

Reactive oxygen species are capable of causing damage to various cellular constituents, such as DNA, proteins and lipids, leading to carcinogenesis, aging and a number of diseases. We have investigated the sequence specificity of oxidative stress-mediated DNA damage by using ^P-labeled DNA fragments obtained from the human c-Ha-ras-1, p53 and p16 genes. The sequence specificity of DNA damage plays the key role in the mutagenic process, and affects the mutation frequency. Therefore, investigation on sequence specificity of DNA damage would provide clues on the biological significance of DNA damage which in turn may be beneficial for cancer prevention strategy. Here we discuss the mechanisms and sequence specificity of DNA damage caused by various environmental chemicals and UVA-activated photosensitizers in relation to carcinogenesis and aging.

Published
2001

45. Quantitation of DNA methylation in Epstein-Barr virus-associated nasopharyngeal carcinoma by bisulfite amplicon sequencing.

Author

Weilin Zhao, Yingxi Mo, Shumin Wang, Kaoru Midorikawa, Ning Ma, Yusuke Hiraku, Shinji Oikawa, Guangwu Huang, Zhe Zhang, Mariko Murata, Kazuhiko Takeuchi, Zhao, Weilin, Mo, Yingxi, Wang, Shumin, Midorikawa, Kaoru, Ma, Ning, Hiraku, Yusuke, Oikawa, Shinji, Huang, Guangwu, and Zhang, Zhe

Subjects
DNA methylation, METHYLATION, CARCINOGENESIS, CARCINOMA, EPSTEIN-Barr virus, DNA microarrays
Abstract

Background: Epigenetic changes, including DNA methylation, disrupt normal cell function, thus contributing to multiple steps of carcinogenesis. Nasopharyngeal carcinoma (NPC) is endemic in southern China and is highly associated with Epstein-Barr virus (EBV) infection. Significant changes of the host cell methylome are observed in EBV-associated NPC with cancer development. Epigenetic marks for NPC diagnosis are urgently needed. In order to explore DNA methylation marks, we investigated DNA methylation of candidate genes in EBV-associated nasopharyngeal carcinoma.Methods: We first employed methyl-capture sequencing and cDNA microarrays to compare the genome-wide methylation profiles of seven NPC tissues and five non-cancer nasopharyngeal epithelium (NNE) tissues. We found 150 hypermethylated CpG islands spanning promoter regions and down-regulated genes. Furthermore, we quantified the methylation rates of seven candidate genes using bisulfite amplicon sequencing for nine NPC and nine NNE tissues.Results: All seven candidate genes showed significantly higher methylation rates in NPC than in NNE tissues, and the ratios (NPC/NNE) were in descending order as follows: ITGA4 > RERG > ZNF671 > SHISA3 > ZNF549 > CR2 > RRAD. In particular, methylation levels of ITGA4, RERG, and ZNF671 could distinguish NPC patients from NNE subjects.Conclusions: We identified the DNA methylation rates of previously unidentified NPC candidate genes. The combination of genome-wide and targeted methylation profiling by next-generation sequencers should provide useful information regarding cancer-specific aberrant methylation. [ABSTRACT FROM AUTHOR]

Published
2017
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48. 酸化ストレスによるクラスターDNA損傷機構とその変異における役割(日本環境変異原学会第32回大会シンポジウム2「DNA損傷と変異のメカニズム」)

Author

三重大学医学部衛生学講座, Department of Environmental and Molecular Medicine, Mie University School of Medicine, Oikawa, Shinji, Ohnishi, Shiho, Murata, Mariko, Hiraku, Yusuke, Kawanishi, Shosuke, 及川, 伸二, 大西, 志保, 村田, 真理子, 平工, 雄介, 川西, 正祐, 三重大学医学部衛生学講座, Department of Environmental and Molecular Medicine, Mie University School of Medicine, Oikawa, Shinji, Ohnishi, Shiho, Murata, Mariko, Hiraku, Yusuke, Kawanishi, Shosuke, 及川, 伸二, 大西, 志保, 村田, 真理子, 平工, 雄介, and 川西, 正祐

Abstract

Reactive oxygen species generated by environmental factors, such as radiation, UV and chemicals can cause sequence-specific DNA damage and play important roles in mutagenesis and carcinogenesis. We have investigated sequence specificity of oxidative stress-mediated DNA damage by using ^<32>P-labeled DNA fragments obtained from the human c-Ha-ras-1, p53 and p16 genes. Free hydroxyl radicals cause DNA damage with no marked site specificity. Copper-hydroperoxo complex caused DNA damage at thymine, cytosine and guanine residues. ^1O_2 preferentially induces lesions at guanine residues. Benzoyloxyl radical specifically causes damage to the 5'-G in GG sequence ; this sequence is easily oxidized because a large part of the highest occupied molecular orbital of this radical is distributed on this site. Recently, we demonstrated that BP-7, 8-dione, a metabolite of carcinogenic benzo [a] pyrene (BP), strongly damaged the G and C of the 5'-ACG-3' sequence complementary to codon 273 of the p53 gene in the presence of NADH and Cu (II). BP-7, 8-dione also caused preferential double base lesion at 5'-TG-3' sequences. Since clustered DNA damage is poorly repaired, it is speculated that induction of the double base lesions in DNA might lead to activation of proto-oncogene or inactivation of the tumor suppressor gene. Therefore, oxidative DNA damage induced by BP-7,8-dione, especially double base lesions, may participate in the expression of carcinogenicity of BP in addition to DNA adduct formation. Here, we discuss the mechanisms of sequence-specific DNA damage including clustered DNA damage in relation to mutagenesis and carcinogenesis.

Published
2008

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