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Transposon Mediated Integration of Plasmid DNA into the Subventricular Zone of Neonatal Mice to Generate Novel Models of Glioblastoma

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Single-cell MultiOmics and spatial transcriptomics demonstrate neuroblastoma developmental plasticity.

Yunyun Xu¹, Daohua Lou², Ping Chen³

¹Pediatric Clinical Research Institute, Children's Hospital Affiliated to Soochow University, Suzhou, Jiangsu 215000, China.

Developmental Cell

|May 10, 2025

Summary

This summary is machine-generated.

Neuroblastoma, a common pediatric cancer, shows developmental plasticity. This study reveals intermediate states and epigenetic priming driving high-risk tumor transitions, offering new therapeutic targets.

Keywords:

development developmental plasticity epigenetic priming gene regulatory network intermediate state intratumoral heterogeneity microenvironment neuroblastoma single-cell MultiOmics spatial transcriptomics

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Published on: August 25, 2020

Area of Science:

Pediatric Oncology
Cancer Biology
Developmental Biology

Background:

Neuroblastoma is the most common extracranial pediatric solid tumor, originating from neural crest cells.
High-risk neuroblastoma has poor survival rates (<50%) due to its developmental plasticity and heterogeneity.
The regulatory mechanisms behind neuroblastoma's plasticity are not well understood.

Purpose of the Study:

To dissect the transcriptional and epigenetic landscapes governing developmental states in neuroblastoma.
To identify key regulatory mechanisms driving malignant transitions in high-risk neuroblastoma.
To explore potential therapeutic strategies targeting transcription factors.

Main Methods:

Utilized single-cell MultiOmics from a mouse spontaneous tumor model.
Employed spatial transcriptomics on human patient samples.
Mapped enhancer gene regulatory networks (eGRNs) and tumor microenvironments.

Main Results:

Identified critical developmental intermediate states in high-risk neuroblastomas.
Uncovered extensive epigenetic priming enabling diverse state transitions.
Mapped eGRNs and tumor microenvironments sustaining aggressive neuroblastoma states.

Conclusions:

Developmental intermediate states and epigenetic priming are key to high-risk neuroblastoma progression.
Targeting transcription factors controlling eGRNs offers a potential therapeutic avenue.
Understanding these regulatory mechanisms can improve neuroblastoma treatment outcomes.