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- W4361245997 abstract "<div>Abstract<p><i>Phosphatase and tensin homologue deleted from chromosome 10</i> (<i>Pten</i>) is expressed aberrantly in non–small cell lung cancer cells, but the role of <i>Pten</i> in lung neoplasia has not been fully elucidated. In this study, we used a genetic approach to inactivate <i>Pten</i> in the bronchial epithelium of mice. Although, by itself, <i>Pten</i> inactivation had no discernible effect on bronchial epithelial histology, it accelerated lung tumorigenesis initiated by oncogenic <i>K-ras</i>, causing more rapid lethality than that induced by oncogenic <i>K-ras</i> alone (8 weeks versus 24 weeks of median duration of survival, respectively). Lung tumors arose in <i>K-ras</i> mutant, <i>Pten</i>-deficient mice that rapidly obstructed bronchial lumina and replaced alveolar spaces. Relative to <i>K-ras</i> mutant tumors, the <i>K-ras</i> mutant, <i>Pten</i>-deficient tumors exhibited more advanced histologic severity and more prominent inflammation and vascularity. Thus, <i>Pten</i> inactivation cooperated with oncogenic <i>K-ras</i> in promoting lung tumorigenesis. [Cancer Res 2008;68(4):1119–27]</p></div>" @default.
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- W4361245997 date "2023-03-30" @default.
- W4361245997 modified "2023-10-16" @default.
- W4361245997 title "Data from <i>Pten</i> Inactivation Accelerates Oncogenic <i>K-ras</i>–Initiated Tumorigenesis in a Mouse Model of Lung Cancer" @default.
- W4361245997 doi "https://doi.org/10.1158/0008-5472.c.6497162.v1" @default.
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