Abstract

Abstract c-MYC is a bHLH transcription factor that heterodimerizes with MAX to form an active transcription factor complex that binds to promoter regions across the genome. MYC is a potent oncogene that promotes tumorigenesis in many cell types. Several studies have shown that tumor cells can be dependent on proto-oncogenes such as MYC, a state called “oncogene addiction.” Recent findings have revealed that c-myc amplifies active gene programs, and our group has previously identified a unique MYC transcriptional signature. In an effort to understand how MYC regulates discrete transcriptional programs across the genome we searched for potential cofactors that coordinate with MYC. Using computational approaches we examined several publically available human data sets as well as our own conditional MYC murine model for potential co-factor interactions. We have determined that several Jumonji family members coordinate with MYC expression. Currently, we are using CRISPR/Cas9 mediated disruption of target genes in murine cells to investigate whether these genes have a casual role in MYC oncogene addiction. Citation Format: Daniel Koch, Stacey Adams, Andrew Gentles, Benedict Anchang, Delaney Sullivan, Sylvia Plevritis, Dean Felsher. Gene expression signatures associated with MYC oncogene addiction in lymphoma. [abstract]. In: Proceedings of the AACR Special Conference on Myc: From Biology to Therapy; Jan 7-10, 2015; La Jolla, CA. Philadelphia (PA): AACR; Mol Cancer Res 2015;13(10 Suppl):Abstract nr A48.

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