ReviewCell and tissue research2018
Neuroblastoma pathogenesis: deregulation of embryonic neural crest development.
Review in Cell and tissue research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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.
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.
Who cites it
65 citing papers in PubMed, 116 citations in OpenAlex.
- A Differentiated SH-SY5Y Model of Hypoxic-Ischaemic Injury Reveals Dynamic Transcriptomic Responses During Reoxygenation.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Article
- Alternative Splicing of the NF-Y Subunit, NF-YA, in Neuroblastoma Phenotype Heterogeneity.Cancers · 2026Review
- Jurkat T-Cell Antigen-Independent Elimination of PMA-Activated Neuroblastoma Cells Is Triggered by CCL2/CCR2, Depends Upon Lipid Raft LFA1/ICAM1 Immune Synapses, Is Mediated by m-TRAIL and Is Augmented by the TrkAIII Oncoprotein.International journal of molecular sciences · 2026Article
- Rho GTPases signaling mediates aggressiveness and differentiation in neuroblastoma tumors.Cell communication and signaling : CCS · 2026Article
- Striking at Survivin: YM-155 Inhibits High-Risk Neuroblastoma Growth and Enhances Chemosensitivity.Cancers · 2025Article
- Multicellular model of neuroblastoma proposes unconventional therapy based on multiple roles of p53.PLoS computational biology · 2024Article
- Review
- Small-molecule inhibition of the METTL3/METTL14 complex suppresses neuroblastoma tumor growth and promotes differentiation.Cell reports · 2024Article
- Molecular Characterization and Inhibition of a Novel Stress-Induced Mitochondrial Protecting Role for Misfolded TrkAIII in Human SH-SY5Y Neuroblastoma Cells.International journal of molecular sciences · 2024Article
- Article
- A peptide encoded by the circular form of the SHPRH gene induces apoptosis in neuroblastoma cells.PeerJ · 2024Article
- Expansion of a neural crest gene signature following ectopic MYCN expression in sympathoadrenal lineage cells in vivo.PloS one · 2024Article
- The intricate interplay between cancer stem cells and cell-of-origin of cancer: implications for therapeutic strategies.Frontiers in oncology · 2024Review
- Epigenetic Dysregulation inInternational journal of molecular sciences · 2023Review
- Neuroblastoma Interaction with the Tumour Microenvironment and Its Implications for Treatment and Disease Progression.Current oncology (Toronto, Ont.) · 2023Review
- Targeting the epigenome of cancer stem cells in pediatric nervous system tumors.Molecular and cellular biochemistry · 2023Review
- Serum brain-derived neurotrophic factor (BDNF) as predictors of childhood neuroblastoma relapse.BMC cancer · 2023Article
- Identification of a novel gene signature for neuroblastoma differentiation using a Boolean implication network.Genes, chromosomes & cancer · 2023Article
- Article
- Mathematical Model of Clonal Evolution Proposes a Personalised Multi-Modal Therapy for High-Risk Neuroblastoma.Cancers · 2023Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Neuroblastoma (NB) is an aggressive pediatric cancer that originates from neural crest tissues of the sympathetic nervous system. NB is highly heterogeneous both from a clinical and a molecular perspective. Clinically, this cancer represents a wide range of phenotypes ranging from spontaneous regression of 4S disease to unremitting treatment-refractory progression and death of high-risk metastatic disease. At a cellular level, the heterogeneous behavior of NB likely arises from an arrest and deregulation of normal neural crest development. In the present review, we summarize our current knowledge of neural crest development as it relates to pathways promoting 'stemness' and how deregulation may contribute to the development of tumor-initiating CSCs. There is an emerging consensus that such tumor subpopulations contribute to the evolution of drug resistance, metastasis and relapse in other equally aggressive malignancies. As relapsed, refractory disease remains the primary cause of death for neuroblastoma, the identification and targeting of CSCs or other primary drivers of tumor progression remains a critical, clinically significant goal for neuroblastoma. We will critically review recent and past evidence in the literature supporting the concept of CSCs as drivers of neuroblastoma pathogenesis.
Indexed as
Identifiers
What OpenQuestion holds
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.