ReviewCell and tissue research2018
Spontaneous regression of neuroblastoma.
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 126 papers, 1 of them a synthesis that pooled 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.
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
126 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Risk factors of neuroblastoma: a systematic review and meta-analysis.Frontiers in public health · 2025Pooled it
- Trial
- Comparative ASCL1 Interactome Analysis Reveals CDK2-Cyclin A2 as Suppressors of Differentiation in MYCN-Amplified Neuroblastoma.Molecular cancer research : MCR · 2026Article
- Multimodal magnetic resonance imaging in neuroblastoma chemotherapy: a narrative review.World journal of surgical oncology · 2026Review
- Conception-calibrated male pediatric tumor mitotic clocks.Communications biology · 2026Article
- Surgical management of pancreatic ganglioneuroma in a child: case report.Journal of surgical case reports · 2026Article
- Regressive Neuroblastoma: Widely Accepted, Underreported Histology.Clinical case reports · 2026Article
- MYCN inhibits TrkC-mediated differentiation in neuroblastoma cells via disruption of the PKA signalling pathway.Cell death discovery · 2026Article
- Aggressive Neuroblastomas Start Growing after Infancy.bioRxiv : the preprint server for biology · 2026Article
- Neuroblastoma in Childhood: Biological Insights, Risk Stratification, and Advances in Multimodal Therapy.Journal of clinical medicine · 2026Review
- YAP1 Enhances Mesenchymal-Type Gene Expression in Human Adrenergic-Type Neuroblastoma Cells.Cancers · 2026Article
- Regulatory Relationships between DNA Methylation and Long Noncoding RNAs in Neuroblastoma.Current medicinal chemistry · 2026Review
- Neuroblastoma in neonates: a case report and literature review.Frontiers in oncology · 2026Article
- Sprouty in Tumors of the Nervous System.International journal of molecular sciences · 2025Review
- Cancer Reversion Therapy: Prospects, Progress and Future Directions.Current issues in molecular biology · 2025Review
- Next-Generation Imaging Techniques for Surgical Guidance in Pediatric Tumors.Annals of surgical oncology · 2025Review
- Fuelling Neuroblastoma: Genomic Analysis of Ketolytic and Glycolytic Gene Expression in Relation to MYCN Oncogene Amplification, Stage and Prognosis.Cancer reports (Hoboken, N.J.) · 2025Article
- The inherent fragility of collective proliferative control.iScience · 2025Article
- m1A methylase TRMT6 promotes neuroblastoma development by demethylating SST mRNA in an m1A/YTHDF2-dependent manner.British journal of cancer · 2025Article
- Moving beyond cytotoxicity in cancer immunotherapy: embracing tumor microenvironment remodeling for durable control.British journal of cancer · 2025Review
66 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
1 author.
Funding
Abstract
Neuroblastomas are characterized by heterogeneous clinical behavior, from spontaneous regression or differentiation into a benign ganglioneuroma, to relentless progression despite aggressive, multimodality therapy. Indeed, neuroblastoma is unique among human cancers in terms of its propensity to undergo spontaneous regression. The strongest evidence for this comes from the mass screening studies conducted in Japan, North America and Europe and it is most evident in infants with stage 4S disease. This propensity is associated with a pattern of genomic change characterized by whole chromosome gains rather than segmental chromosome changes but the mechanism(s) underlying spontaneous regression are currently a matter of speculation. There is evidence to support several possible mechanisms of spontaneous regression in neuroblastomas: (1) neurotrophin deprivation, (2) loss of telomerase activity, (3) humoral or cellular immunity and (4) alterations in epigenetic regulation and possibly other mechanisms. It is likely that a better understanding of the mechanisms of spontaneous regression will help to identify targeted therapeutic approaches for these tumors. The most easily targeted mechanism is the delayed activation of developmentally programmed cell death regulated by the tropomyosin receptor kinase A (TrkA) pathway. Pan-Trk inhibitors are currently in clinical trials and so Trk inhibition might be used as the first line of therapy in infants with biologically favorable tumors that require treatment. Alternative approaches consist of breaking immune tolerance to tumor antigens but approaches to telomere shortening or epigenetic regulation are not easily druggable. The different mechanisms of spontaneous neuroblastoma regression are reviewed here, along with possible therapeutic approaches.
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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.