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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2005-2-16
pubmed:abstractText
Our previous studies of lung cancer in chromate-exposed workers (chromate lung cancer) have revealed that the frequency of replication error (RER) in chromate lung cancer is very high. We examined whether the RER phenotype of chromate lung cancer is due to an abnormality of DNA mismatch repair protein. We investigated the expression of a DNA mismatch repair gene, hMLH1, and hMSH2 proteins using immunohistochemistry and microsatellite instability (MSI) in 35 chromate lung cancers and 26 nonchromate lung cancers. Lung cancer without MSI or with MSI at one locus was defined as "RER(-)," lung cancer with MSI at two loci was defined as "RER(+)," and lung cancer with MSI at three or more loci was defined as "RER(++)." The repression rate of hMLH1 and hMSH2 proteins in chromate lung cancer was significantly more than that of nonchromate lung cancer (hMLH1: 56% vs. 20%, P = 0.006, hMSH2: 74% vs. 23%, P < 0.0001). In chromate lung cancer, the repression rate for hMLH1 was 43% in RER(-), 40% in RER(+), and 90% in the RER(++) group. The repression rate of hMLH1 protein in the RER(++) group was significantly higher than that in the RER(-) and RER(+) groups (P = 0.039). The inactivation of hMLH1 expression strongly correlated with the microsatellite high instability phenotype in chromate lung cancer. The genetic instability of chromate lung cancer is due to the repression of hMLH1 protein.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0899-1987
pubmed:author
pubmed:copyrightInfo
(c) 2004 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:volume
42
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
150-8
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:15605365-Adaptor Proteins, Signal Transducing, pubmed-meshheading:15605365-Adult, pubmed-meshheading:15605365-Aged, pubmed-meshheading:15605365-Base Pair Mismatch, pubmed-meshheading:15605365-Carrier Proteins, pubmed-meshheading:15605365-Chromates, pubmed-meshheading:15605365-DNA Methylation, pubmed-meshheading:15605365-DNA Repair, pubmed-meshheading:15605365-Down-Regulation, pubmed-meshheading:15605365-Gene Expression Regulation, Neoplastic, pubmed-meshheading:15605365-Genomic Instability, pubmed-meshheading:15605365-Humans, pubmed-meshheading:15605365-Lung Neoplasms, pubmed-meshheading:15605365-Male, pubmed-meshheading:15605365-Microsatellite Repeats, pubmed-meshheading:15605365-Middle Aged, pubmed-meshheading:15605365-Neoplasm Proteins, pubmed-meshheading:15605365-Neoplasm Staging, pubmed-meshheading:15605365-Nuclear Proteins, pubmed-meshheading:15605365-Occupational Diseases, pubmed-meshheading:15605365-Occupational Exposure, pubmed-meshheading:15605365-Promoter Regions, Genetic
pubmed:year
2005
pubmed:articleTitle
Microsatellite instability and protein expression of the DNA mismatch repair gene, hMLH1, of lung cancer in chromate-exposed workers.
pubmed:affiliation
Department of Oncological and Regenerative Surgery, Institute of Health Biosciences, University of Tokushima Graduate School, Tokushima City, Japan.
pubmed:publicationType
Journal Article