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Erschienen in: Lung 3/2012

01.06.2012

Heme Oxygenase-1 Promoter Polymorphism is Associated with Risk of Malignant Mesothelioma

verfasst von: Aki Murakami, Yoshihiro Fujimori, Yoshie Yoshikawa, Shusai Yamada, Kunihiro Tamura, Noriko Hirayama, Takayuki Terada, Kozo Kuribayashi, Chiharu Tabata, Kazuya Fukuoka, Tomoko Tamaoki, Takashi Nakano

Erschienen in: Lung | Ausgabe 3/2012

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Abstract

Background

Malignant mesothelioma is an aggressive tumor of serosal surfaces that is closely associated with asbestos exposure which induces oxidative stress. Heme oxygenase (HO)-1, a rate-limiting enzyme of heme degradation, plays a protective role against oxidative stress. The HO-1 gene promoter carries (GT)n repeats whose number is inversely related to transcriptional activity of the HO-1 gene.

Methods

To investigate the relationship between the length polymorphism of (GT)n repeats and mesothelioma susceptibility, we analyzed the HO-1 promoter in 44 asbestos-exposed subjects without mesothelioma and 78 asbestos-exposed subjects with mesothelioma using PCR-based genotyping.

Results

The number of repeats ranged from 16 to 38, with two peaks at 23 and 30 repeats. Polymorphisms of (GT)n repeats were grouped into two classes of alleles, short (S) (<24) and long (L) (≥24), and three genotypes: L/L, L/S, and S/S. The proportions of allele frequencies in class L as well as genotypic frequencies of L allele carriers (L/L and L/S) were significantly higher in the asbestos-exposed subjects with mesothelioma than in those without mesothelioma.

Conclusion

The findings of this study suggest that long (GT)n repeats in the HO-1 gene promoter are associated with a higher risk of malignant mesothelioma in the Japanese population.
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Metadaten
Titel
Heme Oxygenase-1 Promoter Polymorphism is Associated with Risk of Malignant Mesothelioma
verfasst von
Aki Murakami
Yoshihiro Fujimori
Yoshie Yoshikawa
Shusai Yamada
Kunihiro Tamura
Noriko Hirayama
Takayuki Terada
Kozo Kuribayashi
Chiharu Tabata
Kazuya Fukuoka
Tomoko Tamaoki
Takashi Nakano
Publikationsdatum
01.06.2012
Verlag
Springer-Verlag
Erschienen in
Lung / Ausgabe 3/2012
Print ISSN: 0341-2040
Elektronische ISSN: 1432-1750
DOI
https://doi.org/10.1007/s00408-012-9371-2

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