ArticleAdvanced materials (Deerfield Beach, Fla.)2025
Extracellular Matrix Topography Drives Adrenergic to Mesenchymal Transition in Neuroblastoma.
Article in Advanced materials (Deerfield Beach, Fla.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Unveiling the molecular landscape: Long non-coding RNAs in neuroblastoma (Review).Oncology reports · 2026Review
- Nanomedicines Reshape the Tumor Microenvironment: Multidimensional Strategies from Modulating "Barriers" to Metabolic Intervention.International journal of nanomedicine · 2026Review
- Neuroblastoma cell lines display heterogeneity in differentiation responses.Wellcome open research · 2024Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Neuroblastoma (NB), the most common extracranial solid tumor in children, exhibits intra-tumoral heterogeneity with two interconvertible identities: adrenergic (ADRN) and mesenchymal (MES). Compared to ADRN cells, MES cells exhibit phenotypes associated with metastasis and therapy resistance. Thus, the transition from ADRN to MES may contribute to poor clinical outcomes, necessitating further investigation into this ADRN-to-MES transition (AMT) to improve clinical responses. The extracellular matrix (ECM), a critical component of the tumor microenvironment (TME), provides structural support and delivers mechanical signals that influence oncogenic processes. This research demonstrates that high-risk NB tumors contain more topographically aligned ECM fibers than low-risk NB tumors. Using nano-fabricated biomaterials designed to mimic the aligned ECM, ECM topography is revealed to drive AMT through transcriptional and epigenetic changes, accompanied by enhanced MES phenotypic features. Furthermore, ECM topography is shown to stimulate Rho-associated kinase and YAP signaling pathways, which mediate ECM-driven reprogramming. These findings introduce ECM-driven AMT as a novel mechanism in NB progression and provide insights into TME-targeted therapeutic strategies aimed at suppressing MES cells to improve clinical outcomes in NB.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.