Expression signatures of metastatic capacity in a genetic mouse model of lung adenocarcinoma.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 19404390.
- Also identified by DOI 10.1371/journal.pone.0005401 and PMC identifier 2671160.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
BACKGROUND: Non-small cell lung cancer (NSCLC) is the foremost cause of cancer-related death in Western countries, which is due partly to the propensity of NSCLC cells to metastasize. The biologic basis for NSCLC metastasis is not well understood. METHODOLOGY/PRINCIPAL FINDINGS: Here we addressed this deficiency by transcriptionally profiling tumors from a genetic mouse model of human lung adenocarcinoma that develops metastatic disease owing to the expression of K-ras(G12D) and p53(R172H). We identified 2,209 genes that were differentially expressed in distant metastases relative to matched lung tumors. Mining of publicly available data bases revealed this expression signature in a subset of NSCLC patients who had a poorer prognosis than those without the signature. CONCLUSIONS/SIGNIFICANCE: These findings provide evidence that K-ras(G12D); p53(R172H) mice recapitulate features of human NSCLC metastasis and will provide a useful platform on which to study the biologic basis for lung adenocarcinoma metastasis and its prevention by novel agents.
Medical subject headings
- Adenocarcinoma
- Disease Models, Animal
- Lung Neoplasms
- Mutation, Missense
- Neoplasm Metastasis