| http://purl.uniprot.org/citations/18683321 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/18683321 | http://www.w3.org/2000/01/rdf-schema#comment | "Pten is a negative regulator of the Akt pathway, and its inactivation is believed to be an etiological factor in many tumor types. Pten+/-mice are susceptible to a variety of spontaneous tumor types, depending on strain background. Pten+/-mice, in lung tumor-sensitive and -resistant background strains, were treated with a tobacco carcinogen, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), to determine whether allelic Pten deletion can cooperate with NNK in carcinogenesis in lung or other tissues. In lung tumor-resistant C57BL/6 Pten+/- or +/+ mice, NNK treatment did not lead to any lung tumors and did not increase the incidence or severity of tumors previously reported for this strain. In contrast, in a lung tumor-susceptible pseudo-A/J strain, there was a dose-dependent increase in lung tumor size in Pten+/-compared with +/+ mice, although there was no increase in multiplicity. No other tumor types were observed in pseudo-A/J Pten+/-mice regardless of NNK treatment. Lung tumors from these Pten+/-mice had K-ras mutations, retained Pten expression and had similar Akt pathway activation as lung tumors from +/+ mice. Therefore, deletion of a single copy of Pten does not substantially add to the lung tumor phenotype conferred by mutation of K-ras by NNK, and there is likely no selective advantage for loss of the second Pten allele in lung tumor initiation."xsd:string |
| http://purl.uniprot.org/citations/18683321 | http://purl.org/dc/terms/identifier | "doi:10.1593/neo.08406"xsd:string |
| http://purl.uniprot.org/citations/18683321 | http://purl.uniprot.org/core/author | "Han W."xsd:string |
| http://purl.uniprot.org/citations/18683321 | http://purl.uniprot.org/core/author | "Hollander M.C."xsd:string |
| http://purl.uniprot.org/citations/18683321 | http://purl.uniprot.org/core/author | "Anver M.R."xsd:string |
| http://purl.uniprot.org/citations/18683321 | http://purl.uniprot.org/core/author | "Linnoila R.I."xsd:string |
| http://purl.uniprot.org/citations/18683321 | http://purl.uniprot.org/core/author | "Dennis P.A."xsd:string |
| http://purl.uniprot.org/citations/18683321 | http://purl.uniprot.org/core/author | "Balogh A.R."xsd:string |
| http://purl.uniprot.org/citations/18683321 | http://purl.uniprot.org/core/author | "Liwanag J."xsd:string |
| http://purl.uniprot.org/citations/18683321 | http://purl.uniprot.org/core/date | "2008"xsd:gYear |
| http://purl.uniprot.org/citations/18683321 | http://purl.uniprot.org/core/name | "Neoplasia"xsd:string |
| http://purl.uniprot.org/citations/18683321 | http://purl.uniprot.org/core/pages | "866-872"xsd:string |
| http://purl.uniprot.org/citations/18683321 | http://purl.uniprot.org/core/title | "Strain-specific spontaneous and NNK-mediated tumorigenesis in Pten+/- mice."xsd:string |
| http://purl.uniprot.org/citations/18683321 | http://purl.uniprot.org/core/volume | "10"xsd:string |
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