Evidence map›Paper›PMID 40557485›Full record

ArticleAdvanced materials (Deerfield Beach, Fla.)2025

Extracellular Matrix Topography Drives Adrenergic to Mesenchymal Transition in Neuroblastoma.

Antonios Chronopoulos, Chandra Kaladhar Vemula, Vic Zamloot, Ivan Chavez, Rebekah Kennedy, Woochan Kim, Devon Bell, Yuanzhong Pan, Babak Moghimi, Jangho Kim and 2 more

Abstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Antonios ChronopoulosCancer and Blood Disease Institute, Children's Hospital Los Angeles, 4650 Sunset Blvd, Los Angeles, California, 90027, USA.
Chandra Kaladhar VemulaCancer and Blood Disease Institute, Children's Hospital Los Angeles, 4650 Sunset Blvd, Los Angeles, California, 90027, USA.
Vic ZamlootCancer and Blood Disease Institute, Children's Hospital Los Angeles, 4650 Sunset Blvd, Los Angeles, California, 90027, USA.
Ivan ChavezCancer and Blood Disease Institute, Children's Hospital Los Angeles, 4650 Sunset Blvd, Los Angeles, California, 90027, USA.
Rebekah KennedyCancer and Blood Disease Institute, Children's Hospital Los Angeles, 4650 Sunset Blvd, Los Angeles, California, 90027, USA.
Woochan KimDepartment of Convergence Biosystem Engineering, Chonnam National University, 77 Yongbong-ro, Buk-gu, Gwangju, 61186, South Korea.
Devon BellCancer and Blood Disease Institute, Children's Hospital Los Angeles, 4650 Sunset Blvd, Los Angeles, California, 90027, USA.
Yuanzhong PanCancer and Blood Disease Institute, Children's Hospital Los Angeles, 4650 Sunset Blvd, Los Angeles, California, 90027, USA.
Babak MoghimiCancer and Blood Disease Institute, Children's Hospital Los Angeles, 4650 Sunset Blvd, Los Angeles, California, 90027, USA.
Jangho KimDepartment of Convergence Biosystem Engineering, Chonnam National University, 77 Yongbong-ro, Buk-gu, Gwangju, 61186, South Korea.
Shahab AsgharzadehCancer and Blood Disease Institute, Children's Hospital Los Angeles, 4650 Sunset Blvd, Los Angeles, California, 90027, USA.
JinSeok ParkCancer and Blood Disease Institute, Children's Hospital Los Angeles, 4650 Sunset Blvd, Los Angeles, California, 90027, USA.ORCID https://orcid.org/0000-0001-6930-895X

Funding

Tumor microenvironment-dependent therapy resistanceP01CA217959 · NCI · CHILDREN'S HOSP OF PHILADELPHIA · PI Kimberly Stegmaier · 2017 to 2026
$20.7M
CHLA start-up fund, CHLA Core pilot grantMargaret E. Early Medical Research Trust to J.P (PI)NCI NIH HHS P01 CA217959NCI NIH HHS P01 CA217959-01
6 · The paper itself

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.

Indexed as

Epithelial-Mesenchymal TransitionExtracellular MatrixNeuroblastomaAnimalsBiocompatible MaterialsCell Line, TumorHumansrho-Associated KinasesSignal TransductionTumor MicroenvironmentBiocompatible Materialsrho-Associated Kinasesadrenergic to mesenchymal transitionextracellular matrixneuroblastomarho‐kinaseYAP

Identifiers

PMID40557485
PMCPMC12942374

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.