ArticleOncogene2003
Analysis of lung tumorigenesis in chimeric mice indicates the Pulmonary adenoma resistance 2 (Par2) locus to operate in the tumor-initiation stage in a cell-autonomous manner: detection of polymorphisms in the Poli gene as a candidate for Par2.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 32 citations in OpenAlex.
- 129-Derived Mouse Strains Express an Unstable but Catalytically Active DNA Polymerase Iota Variant.Molecular and cellular biology · 2015Article
- Elevated DNA polymerase iota (Poli) is involved in the acquisition of aggressive phenotypes of human esophageal squamous cell cancer.International journal of clinical and experimental pathology · 2015Article
- The error-prone DNA polymerase ι provides quantitative resistance to lung tumorigenesis and mutagenesis in mice.Oncogene · 2014Article
- Mcm10 deficiency causes defective-replisome-induced mutagenesis and a dependency on error-free postreplicative repair.Cell cycle (Georgetown, Tex.) · 2014Article
- Article
- Translesion DNA synthesis in the context of cancer research.Cancer cell international · 2011Article
- Translesion synthesis polymerases in the prevention and promotion of carcinogenesis.Journal of nucleic acids · 2010Article
- Y-family DNA polymerases in mammalian cells.Cellular and molecular life sciences : CMLS · 2009Review
- Mouse genome-wide association mapping needs linkage analysis to avoid false-positive Loci.PLoS genetics · 2009Article
- The Kras2 oncogene and mouse lung carcinogenesis.Medical molecular morphology · 2008Review
- What a difference a decade makes: insights into translesion DNA synthesis.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- UV-B radiation induces epithelial tumors in mice lacking DNA polymerase eta and mesenchymal tumors in mice deficient for DNA polymerase iota.Molecular and cellular biology · 2006Article
- Genetic linkage between Pol iota deficiency and increased susceptibility to lung tumors in mice.Cancer science · 2005Article
- A novel mouse Chromosome 2 congenic strain with obesity phenotypes.Mammalian genome : official journal of the International Mammalian Genome Society · 2004Article
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6 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The Pulmonary adenoma resistance 2 (Par2) locus of the BALB/cByJ mouse, located within 0.5 cM of chromosome 18, is responsible for reducing the mean multiplicity of urethane-induced lung tumors relative to those in C57BL/6J, A/J and C3H/HeJ mice. Thus, BALB/B6-Par2 congenic strain genetically identical to BALB/cByJ except carrying C57BL/6J Par2 alleles develops seven times more tumors than BALB/cByJ. To gain clues for identification of Par2 candidate genes, we analysed lung tumorigenesis in BALB/cByJ<-->BALB.B6-Par2 chimeric animals. Of 100 tumors induced by urethane in 16 chimeras, 82 originated from BALB.B6-Par2 cells, indicating the Par2 phenotype to be cell-autonomous. In addition, the BALB.B6-Par2- and BALB/cByJ-derived tumors were similar in mean size, implying that the phenotype is primarily expressed during initiation rather than in the promotion stage of carcinogenesis. Given these results, we surveyed a comprehensive mouse genome database and physically mapped Par2 within a 2.3 Mbp segment containing three known genes, Poli, Mbd2 and Dcc. Among those, the Poli seemed to be the most reasonable Par2 candidate, since it encodes an extremely error-prone DNA polymerase preferentially incorporating G or T opposite template T in vitro, reminiscent of the Kras2 activation because of an A to G or T point mutation within codon 61 with which most urethane-induced lung tumors are initiated. Indeed, our sequencing of Poli cDNAs from BALB/cByJ, C57BL/6J, A/J and C3H/HeJ lungs revealed 21 BALB/cByJ-specific single-nucleotide polymorphisms in the coding region accompanied by seven amino-acid substitutions and an elevated frequency of alternative splicing, while no polymorphisms associated with tumor susceptibility were found for either Mbd2 or Dcc. Notably, we obtained evidence that BALB/cByJ Par2 alleles may selectively decrease the frequency of Kras2-mutated tumors compared with C57BL/6J alleles. Consequently, the Poli is an intriguing Par2 candidate clearly deserving further evaluation.
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