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Acute lymphoblastic leukemia displays a distinct highly methylated genome

ABSTRACT: Acute lymphoblastic leukemia displays a distinct highly methylated genome

PROVIDER: PRJNA688699 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13329743_1.fastq.gz	Fastqsanger.gz
	SRR13329743_2.fastq.gz	Fastqsanger.gz
	SRR13329744_1.fastq.gz	Fastqsanger.gz
	SRR13329744_2.fastq.gz	Fastqsanger.gz
	SRR13329745_1.fastq.gz	Fastqsanger.gz

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Acute lymphoblastic leukemia displays a distinct highly methylated genome

Project description:DNA methylation is tightly regulated during development and is stably maintained in normal cells. In contrast, the methylome of cancer cells is commonly characterized by a global loss of DNA methylation co-occurring with CpG island hypermethylation. In acute lymphoblastic leukemia (ALL), the commonest childhood cancer, perturbations of CpG methylation have been reported to be associated with genetic disease subtype and outcome, but data examining large cohorts at genome-wide scale are lacking. Here, we performed whole-genome bisulfite sequencing of leukemic cells across multiple subtypes of ALL, leukemia cell lines and normal hematopoietic cells, and show that in contrast to most cancers, ALL samples only exhibit CpG island hypermethylation but minimal global loss of methylation. This was most pronounced in T-ALL and accompanied by an exceptionally broad range of hypermethylation of CpG islands between patients that is influenced by TET2 and DNMT3B. These findings demonstrate that ALL is characterized by an unusually highly methylated genome, and provide insights into the deregulation of methylation in cancer.

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Acute lymphoblastic leukemia displays a distinct highly methylated genome.

Project description:DNA methylation is tightly regulated during development and is stably maintained in healthy cells. In contrast, cancer cells are commonly characterized by a global loss of DNA methylation co-occurring with CpG island hypermethylation. In acute lymphoblastic leukemia (ALL), the commonest childhood cancer, perturbations of CpG methylation have been reported to be associated with genetic disease subtype and outcome, but data from large cohorts at a genome-wide scale are lacking. Here, we performed whole-genome bisulfite sequencing across ALL subtypes, leukemia cell lines and healthy hematopoietic cells, and show that unlike most cancers, ALL samples exhibit CpG island hypermethylation but minimal global loss of methylation. This was most pronounced in T cell ALL and accompanied by an exceptionally broad range of hypermethylation of CpG islands between patients, which is influenced by TET2 and DNMT3B. These findings demonstrate that ALL is characterized by an unusually highly methylated genome and provide further insights into the non-canonical regulation of methylation in cancer.

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