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Title[redir]:
Genetic predisposition to neuroblastoma mediated by a LMO1 super-enhancer polymorphism | Nature
Description:
A causal variant is identified at the LMO1 oncogene locus that drives the genetic association of LMO1 with neuroblastoma susceptibility; the causal SNP disrupts a GATA transcription factor binding site within a tissue-specific super-enhancer element in the first intron of LMO1, thereby affecting LMO1 expression. Polymorphisms at the oncogene LMO1 locus have previously been identified as being highly associated with susceptibility to neuroblastoma, a paediatric cancer. John Maris and colleagues now identify a causal variant at this locus, driving the LMO1 genetic association with neuroblastoma susceptibility. The authors show that the causal single nucleotide polymorphism disrupts a GATA transcription factor binding site in a tissue-specific super-enhancer element within the first intron of LMO1, thereby affecting expression of the LMO1 oncogene. Neuroblastoma is a paediatric malignancy that typically arises in early childhood, and is derived from the developing sympathetic nervous system. Clinical phenotypes range from localized tumours with excellent outcomes to widely metastatic disease in which long-term survival is approximately 40% despite intensive therapy. A previous genome-wide association study identified common polymorphisms at the LMO1 gene locus that are highly associated with neuroblastoma susceptibility and oncogenic addiction to LMO1 in the tumour cells1. Here we investigate the causal DNA variant at this locus and the mechanism by which it leads to neuroblastoma tumorigenesis. We first imputed all possible genotypes across the LMO1 locus and then mapped highly associated single nucleotide polymorphism (SNPs) to areas of chromatin accessibility, evolutionary conservation and transcription factor binding sites. We show that SNP rs2168101 G>T is the most highly associated variant (combined P = 7.47 × 10−29, odds ratio 0.65, 95% confidence interval 0.60–0.70), and resides in a super-enhancer defined by extensive acetylation of histone H3 lysine 27 within the first intron of LMO1. The ancestral G allele that is associated with tumour formation resides in a conserved GATA transcription factor binding motif. We show that the newly evolved protective TATA allele is associated with decreased total LMO1 expression (P = 0.028) in neuroblastoma primary tumours, and ablates GATA3 binding (P < 0.0001). We demonstrate allelic imbalance favouring the G-containing strand in tumours heterozygous for this SNP, as demonstrated both by RNA sequencing (P < 0.0001) and reporter assays (P = 0.002). These findings indicate that a recently evolved polymorphism within a super-enhancer element in the first intron of LMO1 influences neuroblastoma susceptibility through differential GATA transcription factor binding and direct modulation of LMO1 expression in cis, and this leads to an oncogenic dependency in tumour cells.
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Keywords {🔍}
neuroblastoma, article, lmo, google, scholar, pubmed, nature, data, cas, cell, cancer, expression, usa, association, gata, locus, access, extended, tumours, susceptibility, allele, genotype, lines, survival, dna, transcription, snp, jmm, research, analysis, cells, risk, shown, table, foundation, institute, pennsylvania, content, superenhancer, maris, study, single, factor, primary, variants, philadelphia, figure, cases, cookies, john,
Topics {✒️}
updated open-access database nature portfolio permissions reprints privacy policy advertising gene expression omnibus tissue-specific super-enhancer element social media childhood cancer research european-american discovery cohort gene-centric approach identifies genome-wide association studies nature genet nature rev nature protocols 1 h3k27ac chip-seq profiling super series gse65664 cancer research biomedical research gata-family transcription factors relevant accession numbers disease-specific enhancer overlying allele-specific expression differences scientific advice lentiviral vector poz-fhn allele-specific expression measured measuring allele-specific expression nature 469 nature 459 nature 528 nature sequence alignment/map format imputation-based snptest analysis extended data figures oncogenic super-enhancer formed lmo1 super-enhancer polymorphism european-american cohort nih grants r01-ca124709 allele-specific lmo1 expression respective kaplan–meier plot springerlink instant access cis-acting regulatory mechanism author correspondence h3k27ac chip-seq mediator establish super-enhancers censored data points showed significantly worse permissions single nucleotide polymorphism pediatric hematology/oncology
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headline:Genetic predisposition to neuroblastoma mediated by a LMO1 super-enhancer polymorphism
description:A causal variant is identified at the LMO1 oncogene locus that drives the genetic association of LMO1 with neuroblastoma susceptibility; the causal SNP disrupts a GATA transcription factor binding site within a tissue-specific super-enhancer element in the first intron of LMO1, thereby affecting LMO1 expression. Polymorphisms at the oncogene LMO1 locus have previously been identified as being highly associated with susceptibility to neuroblastoma, a paediatric cancer. John Maris and colleagues now identify a causal variant at this locus, driving the LMO1 genetic association with neuroblastoma susceptibility. The authors show that the causal single nucleotide polymorphism disrupts a GATA transcription factor binding site in a tissue-specific super-enhancer element within the first intron of LMO1, thereby affecting expression of the LMO1 oncogene. Neuroblastoma is a paediatric malignancy that typically arises in early childhood, and is derived from the developing sympathetic nervous system. Clinical phenotypes range from localized tumours with excellent outcomes to widely metastatic disease in which long-term survival is approximately 40% despite intensive therapy. A previous genome-wide association study identified common polymorphisms at the LMO1 gene locus that are highly associated with neuroblastoma susceptibility and oncogenic addiction to LMO1 in the tumour cells1. Here we investigate the causal DNA variant at this locus and the mechanism by which it leads to neuroblastoma tumorigenesis. We first imputed all possible genotypes across the LMO1 locus and then mapped highly associated single nucleotide polymorphism (SNPs) to areas of chromatin accessibility, evolutionary conservation and transcription factor binding sites. We show that SNP rs2168101 G>T is the most highly associated variant (combined Pâ=â7.47âÃâ10â29, odds ratio 0.65, 95% confidence interval 0.60â0.70), and resides in a super-enhancer defined by extensive acetylation of histone H3 lysine 27 within the first intron of LMO1. The ancestral G allele that is associated with tumour formation resides in a conserved GATA transcription factor binding motif. We show that the newly evolved protective TATA allele is associated with decreased total LMO1 expression (Pâ=â0.028) in neuroblastoma primary tumours, and ablates GATA3 binding (Pâ<â0.0001). We demonstrate allelic imbalance favouring the G-containing strand in tumours heterozygous for this SNP, as demonstrated both by RNA sequencing (Pâ<â0.0001) and reporter assays (Pâ=â0.002). These findings indicate that a recently evolved polymorphism within a super-enhancer element in the first intron of LMO1 influences neuroblastoma susceptibility through differential GATA transcription factor binding and direct modulation of LMO1 expression in cis, and this leads to an oncogenic dependency in tumour cells.
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headline:Genetic predisposition to neuroblastoma mediated by a LMO1 super-enhancer polymorphism
description:A causal variant is identified at the LMO1 oncogene locus that drives the genetic association of LMO1 with neuroblastoma susceptibility; the causal SNP disrupts a GATA transcription factor binding site within a tissue-specific super-enhancer element in the first intron of LMO1, thereby affecting LMO1 expression. Polymorphisms at the oncogene LMO1 locus have previously been identified as being highly associated with susceptibility to neuroblastoma, a paediatric cancer. John Maris and colleagues now identify a causal variant at this locus, driving the LMO1 genetic association with neuroblastoma susceptibility. The authors show that the causal single nucleotide polymorphism disrupts a GATA transcription factor binding site in a tissue-specific super-enhancer element within the first intron of LMO1, thereby affecting expression of the LMO1 oncogene. Neuroblastoma is a paediatric malignancy that typically arises in early childhood, and is derived from the developing sympathetic nervous system. Clinical phenotypes range from localized tumours with excellent outcomes to widely metastatic disease in which long-term survival is approximately 40% despite intensive therapy. A previous genome-wide association study identified common polymorphisms at the LMO1 gene locus that are highly associated with neuroblastoma susceptibility and oncogenic addiction to LMO1 in the tumour cells1. Here we investigate the causal DNA variant at this locus and the mechanism by which it leads to neuroblastoma tumorigenesis. We first imputed all possible genotypes across the LMO1 locus and then mapped highly associated single nucleotide polymorphism (SNPs) to areas of chromatin accessibility, evolutionary conservation and transcription factor binding sites. We show that SNP rs2168101 G>T is the most highly associated variant (combined Pâ=â7.47âÃâ10â29, odds ratio 0.65, 95% confidence interval 0.60â0.70), and resides in a super-enhancer defined by extensive acetylation of histone H3 lysine 27 within the first intron of LMO1. The ancestral G allele that is associated with tumour formation resides in a conserved GATA transcription factor binding motif. We show that the newly evolved protective TATA allele is associated with decreased total LMO1 expression (Pâ=â0.028) in neuroblastoma primary tumours, and ablates GATA3 binding (Pâ<â0.0001). We demonstrate allelic imbalance favouring the G-containing strand in tumours heterozygous for this SNP, as demonstrated both by RNA sequencing (Pâ<â0.0001) and reporter assays (Pâ=â0.002). These findings indicate that a recently evolved polymorphism within a super-enhancer element in the first intron of LMO1 influences neuroblastoma susceptibility through differential GATA transcription factor binding and direct modulation of LMO1 expression in cis, and this leads to an oncogenic dependency in tumour cells.
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