Suppression of Lung Adenocarcinoma Progression by Nkx2-1

ABSTRACT: Despite the high prevalence and poor outcome of patients with metastatic lung cancer, the mechanisms of tumour progression and metastasis remain largely uncharacterized. We modelled human lung adenocarcinoma, which frequently harbours activating point mutations in KRAS1 and inactivation of the p53-pathway2, using conditional alleles in mice3-5. Lentiviral-mediated somatic activation of oncogenic Kras and deletion of p53 in the lung epithelial cells of KrasLSL-G12D/+;p53flox/flox mice initiates lung adenocarcinoma development4. Although tumours are initiated synchronously by defined genetic alterations, only a subset become malignant, suggesting that disease progression requires additional alterations. Identification of the lentiviral integration sites allowed us to distinguish metastatic

ORGANISM(S): Mus musculus

SUBMITTER: Charles Whittaker 

PROVIDER: E-GEOD-26874 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress