Stage-specific sensitivity to p53 restoration in lung cancer: tumor data

ABSTRACT: Tumorigenesis is a multistep process that results from the sequential accumulation of mutations in key oncogene and tumor-suppressor pathways. The quest to personalize cancer medicine based on targeting these underlying genetic abnormalities presupposes that sustained inactivation of tumor suppressors and activation of oncogenes are required for tumor maintenance. Mutations in the p53 tumor-suppressor pathway are a hallmark of cancer and significant efforts toward pharmaceutical reactivation of mutant p53 pathways are underway1-3. Here we show that restoration of p53 in established murine lung tumors leads to significant but incomplete tumor cell loss specifically in malignant adenocarcinomas but not in adenomas. Also, we define amplification of MAPK signaling as a critical determinant of

ORGANISM(S): Mus musculus

SUBMITTER: Charles Whittaker 

PROVIDER: E-GEOD-23874 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress