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Clinically significant copy number alterations and complex rearrangements of MYB and NFIB in adenoid cystic carcinoma of the head and neck

ABSTRACT: Using high-resolution, array-based comparative genomic hybridization (aCGH), we explored genomic alterations in 40 fresh-frozen ACC samples, the largest cohort to date, with the aims to: (1) identify recurrent CNAs in ACC; (2) identify novel candidate target genes; and (3) correlate recurrent CNAs with tumour grade and other clinical parameters to identify potential clinically useful biomarkers.

ORGANISM(S): Homo sapiens

PROVIDER: GSE34816 | GEO | 2012/12/31

SECONDARY ACCESSION(S): PRJNA150261

REPOSITORIES: GEO

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Clinically significant copy number alterations and complex rearrangements of MYB and NFIB in adenoid cystic carcinoma of the head and neck

Project description:Using high-resolution, array-based comparative genomic hybridization (aCGH), we explored genomic alterations in 40 fresh-frozen ACC samples, the largest cohort to date, with the aims to: (1) identify recurrent CNAs in ACC; (2) identify novel candidate target genes; and (3) correlate recurrent CNAs with tumour grade and other clinical parameters to identify potential clinically useful biomarkers. High-resolution aCGH on fresh frozen tissue from 40 ACCs.

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Project description:Translocation events are frequent in cancer and may create chimeric fusions or ‘regulatory rearrangements’ that drive oncogene overexpression. Here we identify super-enhancer translocations that drive overexpression of the oncogenic transcription factor MYB as a recurrent theme in adenoid cystic carcinoma (ACC). Whole-genome sequencing data and chromatin maps reveal distinct chromosomal rearrangements that juxtapose super-enhancers to the MYB locus. Chromosome conformation capture confirms that the translocated enhancers interact with the MYB promoter. Remarkably, MYB protein binds to the translocated enhancers, creating a positive feedback loop that sustains its expression. MYB also binds enhancers that drive different regulatory programs in alternate cell lineages in ACC, cooperating with TP63 in myoepithelial cells and a Notch program in luminal epithelial cells. Bromodomain inhibitors slow tumor growth in ACC primagraft models in vivo. Thus, our study identifies super-enhancer translocations that drive MYB expression and provides insight into downstream MYB functions in the alternate ACC lineages.

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Project description:Translocations that drive overexpression of the oncogenic transcription factor MYB are molecular hallmarks of adenoid cystic carcinoma (ACC), a malignant salivary gland tumor. Surgical resection, whenever possible, is the standard therapy for ACC, but there are no available therapeutic options available if surgery fails. Here we performed a chemical genetic screen using a zebrafish embryo culture system and identified retinoic acid agonists as potent suppressors of c-myb. Retinoic acid treatment strongly decreased c-myb gene expression in U937 cells and suggested a direct transcriptional mechanism of regulation. Retinoic acid agonists strongly inhibited tumor growth in vivo in different ACC patient derived xenograft models. Analysis of the xenografts revealed a significant decrease in MYB binding at translocated enhancers, thereby disrupting the MYB positive feedback loop that drives ACC. Our findings identify an important role of retinoic acid in MYB regulation and as a potential new effective therapy for ACC.

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