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Microsatellite gene instability and abnormality of mismatch gene proteins in human lung cancer from chromate-exposed workers

Research Project

Project/Area Number 10470276
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypeSingle-year Grants
Section一般
Research Field Thoracic surgery
Research InstitutionThe University of Tokushima

Principal Investigator

MONDEN Yasumasa  MD, PhD, Professor, Second Department of Surgery, School of Medicine, The University of Tokushima, 医学部, 教授 (60028628)

Co-Investigator(Kenkyū-buntansha) KONDO Kazuya  MD, PhD, Assistant Professor, Second Department of Surgery, School of Medicine, The University of Tokushima, 医学部, 講師 (10263815)
三好 孝典  徳島大学, 医学部附属病院, 医員(臨床)
Project Period (FY) 1998 – 1999
Project Status Completed (Fiscal Year 1999)
Budget Amount *help
¥10,000,000 (Direct Cost: ¥10,000,000)
Fiscal Year 1999: ¥4,700,000 (Direct Cost: ¥4,700,000)
Fiscal Year 1998: ¥5,300,000 (Direct Cost: ¥5,300,000)
KeywordsChromate lung cancer / Microsatellite instability / loss of heterozygosity / Mismatch repair gene / hMLH1 hMSH2
Research Abstract

Our previous study for human lung cancer from chromate-exposure workers have revealed that chromate exposure induce the particular mutation pattern in the p53 gene of human lung cancer (Biochem Biophys Res Com 139, 95-100, 1997). In this study, we examined the genomic instability in 40 Lung cancers from 33 chromate-exposure workers and 29 lung cancers patients without chromate exposure (control samples) using 6 microsatellite markers. Thirty (75.0%) of the 40 tumors with chromate exposure showed RER+. On the other hand, only 4 (13.3%) of the 29 tumors without chromate exposure showed the replication error-positive phenotype (RER+). The frequency of RER+ in tumors with chromate exposure was higher than that in tumors without chromate exposure (p<0.0001). Moreover, the duration of chromate exposure but not Brinkman index may be associated with numbers of MSI positive.
To clarify the relationship between RER+ and the abnormality of mismatch repair gene, we examined the expressions of hMLH1 and hMSH2 protein in 28 chromate lung cancers and 28 non-chromate lung cancers by immunohistochemistry. All 28 non-chromate lung cancers strongly expressed both hMLH1 and hMSH proteins. On the other hand, 14 (50%) of 28 chromate lung cancers moderately or weakly expressed hMLH protein. Eight (29%) of 28 chromate lung cancers moderately or weakly expressed hMSH protein. It is possible that RER+ in chromate lung cancer may be due to the abnormality of mismatch repair genes.

Report

(3 results)
  • 1999 Annual Research Report   Final Research Report Summary
  • 1998 Annual Research Report

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Published: 1998-03-31   Modified: 2016-04-21  

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