1995 Fiscal Year Final Research Report Summary
Epidemiological and molecular genetic study for environmental and occupational cancers.
| Project/Area Number |
06454235
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Public health/Health science
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| Research Institution | University of Tsukuba |
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Principal Investigator |
HARADA Shoji Institute of Community Medicine, University of Tsukuba Associate Professor, 社会医学系, 助教授 (60086618)
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| Co-Investigator(Kenkyū-buntansha) |
SAGAI Masaru National Institute for Environmental Studies, 地域総合部門, 総合研究官
MURAKAMI Masataka Institute of Community Medicine, University of Tsukuba Professor, 社会医学系, 教授 (30010078)
SHIMOJO Nobuhiro Institute of Community Medicine, University of Tsukuba Professor, 社会医学系, 教授 (00080622)
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| Project Period (FY) |
1994 – 1995
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| Keywords | GSTM1 gene deletion / CYP1A1 / polymorphism / lung cancer / genetic association / case control study / genetic risk factor / Xenobiotics |
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| Research Abstract |
Individual susceptibility to lung cancer due to occupational and environmental exposures to carcinogenetic agents has been shown to be modulated by host-specific factors with genetic background. Recent studies have suggested that inherited differences in metabolic capacity may play a primary role in susceptibility to environmentally induced cancers. In this respect, polymorphic alleles of Glutathione S-Transferase (GSTM1) which is important in the detoxification of several carcinogens, and of Cytochrome P450 1A1 (CYP1A1) which is biotransforming enzymes, were analyzed in the context of the relationship between controls and lung cancer. Blood samples of the 104 controls and 172 patients were collected from peoples living in Sheng-Yan district of People's Republic of China.PCR and related techniques were used for detection of these polymorphic loci.
1) The frequencies of GSTM1 gene deletion was significantly higher in the patients with lung cancer than in controls (P<0.05). In addition, s
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mall cell carcinoma showed the highest association with GSTM1 gene deletion compared with other types of lung cancers such as squamous cell carcinoma and adenocarcinoma.
2) The risk of lung cancer is dependent on the extent of the tobacco smoke exposure. This was supposed by our study showing progressive increase in the proportion of the GSTM1 gene deletion in relation to smoking index, in both squamous (P<0.05) and small cell carcinoma groups (P<0.01).
3) The different frequencies of GSTM1 gene deletion was observed between the patients under 50 years (85.3%) and over 50 years old (61.8%), which are significantly different (P<0.05). Such observation may be associated with onset of lung cancer. Further study will be necessary to confirm association with onset with onset of lung cancer.
4) Several studies have shown that CYP1A1^<**>2 gene is associated with an increased risk of cigarette smoke-induced lung cancer. However, the difference of frequency between the patients with lung cancer and the controls was not significant in our samples. Less
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