Article Abstract:
Analysis of lung tumor growth using conditional expression of oncogenic K-ras is discussed in this research communication. A new model of pulmonary adenocarcinoma (PA) in mice with a conditionally activatable allele of oncogenic K-ras has been developed. Use of a recombinant adenovirus expressing Cre recombinase to bring on K-ras G12D expression in mouse lungs makes possible controls of timing and multiplicity of tumor initiation. A new cell type that helps development of PA was found.
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Article Abstract:
The role in cancer of the membrane/cytoskeleton interface is not well understood. A small spectrum of benign tumors occur in human NF2 (neurofibromatosis type II) patients, but Nf2 heterozygous mice get various malignant tumors. Evidence suggests that Nf2 loss plays a role in metastatic potential. It appears that the NF2 tumor suppressor has a role in tumor formation and metastasis. The ezrin/radixin/moesin (ERM) family of linker proteins may also be a factor.
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Article Abstract:
The phenotype of a mouse engineered to harbor a germline oncogenic K-ras mutation is described. It is found that the Ras/MAPK (mitogen-activated protein kinase) antagonist Sprouty-2 acts as a tumor suppressor in K-ras mediated lung tumorigenesis and regulates the functioning in the pathogenesis of the Ras disease.
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