Abstract
Understanding the aberrant transcriptional landscape of neuroblastoma is necessary to provide insight to the underlying influences of the initiation, progression and persistence of this developmental cancer. Here, we present chromatin immunoprecipitation sequencing (ChIP-Seq) data for the oncogenic transcription factors, MYCN and MYC, as well as regulatory histone marks H3K4me1, H3K4me3, H3K27Ac, and H3K27me3 in ten commonly used human neuroblastoma-derived cell line models. In addition, for all of the profiled cell lines we provide ATAC-Seq as a measure of open chromatin. We validate specificity of global MYCN occupancy in MYCN amplified cell lines and functional redundancy of MYC occupancy in MYCN non-amplified cell lines. Finally, we show with H3K27Ac ChIP-Seq that these cell lines retain expression of key neuroblastoma super-enhancers (SE). We anticipate this dataset, coupled with available transcriptomic profiling on the same cell lines, will enable the discovery of novel gene regulatory mechanisms in neuroblastoma.
Highlights
Background & SummaryAn estimated 15,780 children in the United States will be diagnosed with cancer in 20191
Neuroblastoma shows wide phenotypic variability, with tumors arising in children diagnosed under the age of 18 months often spontaneously regressing with little or no treatment, but patients diagnosed at an older age or with unfavorable genomic features often showing a relentlessly progressive and widely metastatic disease pattern despite intensive, multimodal therapy
Ninety-eight percent of low-risk neuroblastoma disease are currently cured[5], the survival rate for patients with high-risk neuroblastoma remains less than 50%6
Summary
An estimated 15,780 children in the United States will be diagnosed with cancer in 20191. While 80% of pediatric cancer patients overcome this disease, 20% of children do not survive, and survivors often have multiple side effects of therapy[1]. MYCN amplification occurs in nearly 20% of all neuroblastomas, and approximately 50% of patients with high-risk disease[8,9]. It is a truncal genomic event, and typically stable across the spectrum of therapy and disease recurrence. Neuroblastoma tumors with MYCN amplification typically lack or have low MYC mRNA expression[9]. All of the cell lines here have RNA sequencing data freely available[16]
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