Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Gene Expression profiling of Myc-induced lymphomagenesis


ABSTRACT: The ability of oncogenes to provoke cancer is harnessed by regulators that control cell proliferation or induce apoptosis, and bypass of these checkpoints is a hallmark of malignancies. Myc oncoproteins are overexpressed in ~70% of all cancers and induce numerous transcription targets that regulate cell growth, metabolism, and the ribosome machinery. We used the Eμ-Myc mouse model from which one can directly compare expression profiles of wild type versus Myc-expressing B220+ pre-malignant lymphocytes and also queried differences in gene expression that ensue following the neoplastic switch to lymphoma (Nilsson et al., 2005 - PMID:15894264 and Keller et al. 2010 - PMID:20598117). Wild type and precancerous Eμ-Myc transgenic B cells (from 4-6 week old littermates), and lymphomas from 13 independent Eμ-Myc mice were investigated. These samples were used for subsequent RNA purification, labeling and hybridization to MOE430A Affymetrix arrays.

ORGANISM(S): Mus musculus

SUBMITTER: John Cleveland 

PROVIDER: E-GEOD-32239 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications


The functions of key oncogenic transcription factors independent of context have not been fully delineated despite our richer understanding of the genetic alterations in human cancers. The MYC oncogene, which produces the Myc transcription factor, is frequently altered in human cancer and is a major regulatory hub for many cancers. In this regard, we sought to unravel the primordial signature of Myc function by using high-throughput genomic approaches to identify the cell-type independent core M  ...[more]

Publication: 1/3

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