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Defining tumor-associated vascular heterogeneity in pediatric high-grade and diffuse midline gliomas

ABSTRACT: Defining tumor-associated vascular heterogeneity in pediatric high-grade and diffuse midline gliomas

PROVIDER: PRJNA743363 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15031829.fastq.gz	Fastqsanger.gz
	SRR15031830.fastq.gz	Fastqsanger.gz
	SRR15031831.fastq.gz	Fastqsanger.gz
	SRR15031832.fastq.gz	Fastqsanger.gz
	SRR15031833.fastq.gz	Fastqsanger.gz

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Defining tumor-associated vascular heterogeneity in pediatric high-grade and diffuse midline gliomas

Project description:The blood-brain barrier (BBB) plays important roles in brain tumor pathogenesis and treatment response, yet our understanding of its function and heterogeneity within or across brain tumor types remains poorly characterized. Here we analyze the neurovascular unit (NVU) of pediatric high-grade glioma (pHGG) and diffuse midline glioma (DMG) using patient derived xenografts and natively forming glioma mouse models. We show tumor-associated vascular differences between these glioma subtypes, and parallels between PDX and mouse model systems, with DMG models maintaining a more normal vascular architecture, BBB function and endothelial transcriptional program relative to pHGG models. Unlike prior work in angiogenic brain tumors, we find that expression of secreted Wnt antagonists do not alter the tumor-associated vascular phenotype in DMG tumor models. Together, these findings highlight vascular heterogeneity between pHGG and DMG and differences in their response to alterations in developmental BBB signals that may participate in driving these pathological differences.

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Project description:Pediatric low-grade gliomas (PLGGs) are among the most common solid tumors in children but apart from BRAF mutations or duplications in specific subclasses, few genetic driver events are known. Diffuse PLGGs comprise a set of uncommon subtypes that exhibit invasive growth and are therefore especially challenging clinically. These tumors are particularly poorly understood. We performed high-resolution copy-number analysis of 44 diffuse PLGGs to identify recurrent alterations. Diffuse PLGGs exhibited fewer such alterations than adult low-grade gliomas, but we identified several significantly recurrent events. The most significant event, 8q13.1 gains, were observed in 28% of diffuse astrocytomas grade II (DA2s) and resulted in partial duplication of the transcription factor MYBL1 with truncation of its C-terminal negative-regulatory domain. A similar recurrent deletion-truncation breakpoint was identified in two angiocentric gliomas in the related gene MYB on 6q23.3. Whole-genome sequencing of a MYBL1-rearranged DA2 demonstrated MYBL1 tandem duplication, and few other events. Two novel, truncated MYBL1 transcripts identified in this tumor induced anchorage-independent growth when expressed in 3T3 cells and tumor formation in nude mice. Truncated transcripts were also expressed in two additional tumors with MYBL1 partial duplication. Our results define clinically relevant molecular subclasses of diffuse PLGGs and highlight a potential role for the MYB family in the biology of low-grade gliomas.

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