Document Detail


A functional switch from lung cancer resistance to susceptibility at the Pas1 locus in Kras2LA2 mice.
MedLine Citation:
PMID:  16823377     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Pulmonary adenoma susceptibility 1 (Pas1) is the major mouse lung cancer susceptibility locus on chromosome 6 (ref. 1). Kras2 is a common target of somatic mutation in chemically induced mouse lung tumors and is a candidate Pas1 gene. M. spretus mice (SPRET/Ei) carry a Pas1 resistance haplotype for chemically induced lung tumors. We demonstrate that the SPRET/Ei Pas1 allele is switched from resistance to susceptibility by fixation of the parental origin of the mutant Kras2 allele. This switch correlates with low expression of endogenous Kras2 in SPRET/Ei. We propose that the Pas1 modifier effect is due to Kras2, and that a sensitive balance between the expression levels of wild-type and mutant alleles determines lung tumor susceptibility. These data demonstrate that cancer predisposition should also be considered in the context of somatic events and could have major implications for the design of human association studies to identify cancer susceptibility genes.
Authors:
Minh D To; Jesus Perez-Losada; Jian-Hua Mao; Jeff Hsu; Tyler Jacks; Allan Balmain
Related Documents :
2994377 - Effect of the radioprotector wr 2721 on the response of metastatic lewis lung carcinoma...
22173907 - An improved decision support system for detection of lesions in mammograms using differ...
2023697 - Aflatoxins in sera from patients with lung cancer.
9468557 - A human lung cancer xenograft producing granulocyte-colony stimulating factor and parat...
8365317 - Association of miliary lung metastases and bone metastases in bronchogenic carcinoma.
22642827 - Relationships between the abo blood group snp rs505922 and breast cancer phenotypes: a ...
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2006-07-02
Journal Detail:
Title:  Nature genetics     Volume:  38     ISSN:  1061-4036     ISO Abbreviation:  Nat. Genet.     Publication Date:  2006 Aug 
Date Detail:
Created Date:  2006-07-28     Completed Date:  2006-09-11     Revised Date:  2010-12-03    
Medline Journal Info:
Nlm Unique ID:  9216904     Medline TA:  Nat Genet     Country:  United States    
Other Details:
Languages:  eng     Pagination:  926-30     Citation Subset:  IM    
Affiliation:
University of California San Francisco (UCSF) Comprehensive Cancer Center, San Francisco, California 94115, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Adenoma / chemically induced,  genetics
Alleles
Animals
Carcinogens / toxicity
Female
Genetic Predisposition to Disease
Lung Neoplasms / chemically induced,  genetics*
Male
Mice
Models, Genetic
Mutation
Oncogenes
Proto-Oncogene Proteins p21(ras) / genetics*
Risk Factors
Urethane / toxicity
Grant Support
ID/Acronym/Agency:
R01 CA111834-01A2/CA/NCI NIH HHS; R01 CA111834-02/CA/NCI NIH HHS; R01 CA111834-03/CA/NCI NIH HHS; R01 CA111834-04/CA/NCI NIH HHS; U01CA84244/CA/NCI NIH HHS; U01CA84306/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Carcinogens; 51-79-6/Urethane; EC 3.6.5.2/Kras2 protein, mouse; EC 3.6.5.2/Proto-Oncogene Proteins p21(ras)
Comments/Corrections
Comment In:
Nat Genet. 2006 Aug;38(8):864-5   [PMID:  16874325 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  A sequence-oriented comparison of gene expression measurements across different hybridization-based ...
Next Document:  The genetic basis for differences in leaf form between Arabidopsis thaliana and its wild relative Ca...