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Carcinogenesis Advance Access published online on October 7, 2004
Carcinogenesis, doi:10.1093/carcin/bgh299
© 2004 by Oxford University Press
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Received July 30, 2004
Revised September 27, 2004
Accepted September 27, 2004

COMMENTARY

Pas1 haplotype-dependent genetic predisposition to lung tumorigenesis in rodents: a meta-analysis

Giacomo Manenti 1 and Tommaso A. Dragani 1*

1 Department of Experimental Oncology, Istituto Nazionale Tumori, Milan, Italy

* To whom correspondence should be addressed. E-mail: dragani{at}istitutotumori.mi.it.


  Abstract

Rodent species and strains show wide variations in susceptibility to lung tumorigenesis. In mice, hierarchical clustering of 29 laboratory inbred strains by the pulmonary adenoma susceptibility 1 (Pas1) locus polymorphisms separated the strains into either an A/J- or a C57BL/6J-type Pas1 haplotype. A pooled analysis (including >8,500 mice) of studies on spontaneous or chemically-induced lung tumorigenesis in these strains revealed a significantly higher risk of spontaneous lung tumors (odds ratio, OR: 12.17; 95% CI 9.00-16.45) as well as of chemically-induced lung tumors (OR: 15.14; 95% CI 12.51-18.31) in the A/J-type haplotype. Strain differences were observed with six different carcinogens, suggesting that the Pas1 locus activity is carcinogen-independent. Thus, the present meta-analysis indicates a link between the genetic control of spontaneous and chemically-induced lung tumor susceptibility in mice. The Pas1 susceptibility allele is frequent in the population of mouse inbred strains, whereas a counterpart in populations of rat and hamster strains appears to be absent or rare. These findings might help in the interpretation of results of rodent carcinogenicity bioassays and assessing the risk of lung carcinogenesis from chemicals.

Keywords: genetic susceptibility; inbred strains; lung tumors; Kras2; risk assessment.
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