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Cancer-Specific Epigenome Identifies Oncogenic Hijacking by Nuclear Factor I Family Proteins for Medulloblastoma Progression

ABSTRACT: Cancer-Specific Epigenome Identifies Oncogenic Hijacking by Nuclear Factor I Family Proteins for Medulloblastoma Progression

PROVIDER: PRJNA1003431 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25570200_1.fastq.gz	Fastqsanger.gz
	SRR25570200_2.fastq.gz	Fastqsanger.gz
	SRR25570201_1.fastq.gz	Fastqsanger.gz
	SRR25570201_2.fastq.gz	Fastqsanger.gz
	SRR25570202_1.fastq.gz	Fastqsanger.gz

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Dynamic Chromatin Alteration Induces Oncogenic Hijacking by Nuclear Factor I Family Proteins for Medulloblastoma Progression

Project description:The cancer-specific epigenome is the critical scaffold on which genetic programs work to positively promote cancer growth and progression. Understanding and appropriately disrupting this epigenome will lead to the discovery of new, more extensive and effective therapies in addition to conventional personalized medicine that relies on genomic mutations. However, the epigenomic changes during the process from normal cells to cancer formation as well as the molecules involved in the maintenance of the aberrant epigenome are still poorly characterized, and the development of epigenome-based therapeutics is therefore undeniably stagnant. To address this issue, we here focus on SHH-subgroup medulloblastoma, a representative pediatric brain tumor for which we developed a reliable mouse model to capture the epigenomic changes that cerebellar granule cells, the cells of origin, undergo during tumorigenesis. By comparing the epigenomes of the different stages of transforming cells, we identified NFI family of developmental factors as oncogenic regulators in the epigenome of pre-cancerous and cancerous cells, which they also contribute to maintain. Furthermore, we report pharmacological experiments demonstrating that inhibition of NFIB methylation blocks tumor growth and increases sensitivity to molecularly targeted drugs by disrupting the cancer epigenome. Thus, this study is a unique example of how epigenomic studies of cancer have led directly to therapeutic insights, and similar approaches in various cancers would accelerate the establishment of novel therapies.

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Dynamic Chromatin Alteration Induces Oncogenic Hijacking by Nuclear Factor I Family Proteins for Medulloblastoma Progression

Project description:Dynamic Chromatin Alteration Induces Oncogenic Hijacking by Nuclear Factor I Family Proteins for Medulloblastoma Progression

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Dynamic Chromatin Alteration Induces Oncogenic Hijacking by Essential Transcriptional Factors during Medulloblastoma Tumorigenesis [Multiome]

Project description:Dynamic Chromatin Alteration Induces Oncogenic Hijacking by Essential Transcriptional Factors during Medulloblastoma Tumorigenesis [Multiome]

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Cancer-Specific Epigenome Identifies Oncogenic Hijacking by Nuclear Factor I Family Proteins for Medulloblastoma Progression

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-05-03 | GSE240362 | GEO

Dynamic Chromatin Alteration Induces Oncogenic Hijacking by Essential Transcriptional Factors during Medulloblastoma Tumorigenesis [ATAC-Seq]

Project description:Dynamic Chromatin Alteration Induces Oncogenic Hijacking by Essential Transcriptional Factors during Medulloblastoma Tumorigenesis [ATAC-Seq]

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Dynamic Chromatin Alteration Induces Oncogenic Hijacking by Essential Transcriptional Factors during Medulloblastoma Tumorigenesis [CUT&Tag]

Project description:Dynamic Chromatin Alteration Induces Oncogenic Hijacking by Essential Transcriptional Factors during Medulloblastoma Tumorigenesis [CUT&Tag]

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Dynamic Chromatin Alteration Induces Oncogenic Hijacking by Essential Transcriptional Factors during Medulloblastoma Tumorigenesis [[CUT&Tag 2]

Project description:Dynamic Chromatin Alteration Induces Oncogenic Hijacking by Essential Transcriptional Factors during Medulloblastoma Tumorigenesis [[CUT&Tag 2]

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Transcription profiling of mouse with Hedgehog-induced medulloblastoma reveals oncogenic Hedgehog signaling promotes medulloblastoma from lineage-restricted granule cell progenitors

Project description:Origins of the brain tumor, medulloblastoma, from stem cells or restricted pro-genitor cells are unclear. To investigate this, we activated oncogenic Hedgehog signaling in multipotent and lineage-restricted CNS progenitors. We observed that normal unipo-tent cerebellar granule neuron precursors (CGNP) derive from hGFAP+ and Olig2+ rhombic lip progenitors. Hedgehog activation in a spectrum of early and late stage CNS progenitors generated similar medulloblastomas, but not other brain cancers, indicating that acquisition of CGNP identity is essential for tumorigenesis. We show in human and mouse medulloblastoma that cells expressing the glia-associated markers Gfap and Olig2 are neoplastic and that they retain features of embryonic-type granule lineage progenitors. Thus, oncogenic Hedgehog signaling promotes medulloblastoma from lineage-restricted granule cell progenitors. Gene expression profiling of cerebellar tumors generated from various early and late stage CNS progenitor cells. Experiment Overall Design: Group comparisons with biological replicates

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Enhancer hijacking activates GFI1 family oncogenes in medulloblastoma.

Project description:Medulloblastoma is a highly malignant paediatric brain tumour currently treated with a combination of surgery, radiation and chemotherapy, posing a considerable burden of toxicity to the developing child. Genomics has illuminated the extensive intertumoral heterogeneity of medulloblastoma, identifying four distinct molecular subgroups. Group 3 and group 4 subgroup medulloblastomas account for most paediatric cases; yet, oncogenic drivers for these subtypes remain largely unidentified. Here we describe a series of prevalent, highly disparate genomic structural variants, restricted to groups 3 and 4, resulting in specific and mutually exclusive activation of the growth factor independent 1 family proto-oncogenes, GFI1 and GFI1B. Somatic structural variants juxtapose GFI1 or GFI1B coding sequences proximal to active enhancer elements, including super-enhancers, instigating oncogenic activity. Our results, supported by evidence from mouse models, identify GFI1 and GFI1B as prominent medulloblastoma oncogenes and implicate 'enhancer hijacking' as an efficient mechanism driving oncogene activation in a childhood cancer.

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