Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (755 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Malignant neoplasms arising in the neuroectoderm, the portion of the ectoderm of the early embryo that gives rise to the central and peripheral nervous systems, including some glial cells.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Neuroectodermal Tumor; Tumor, Neuroectodermal; Tumors, Neuroectodermal.
Where it fits in the MeSH classification
- Broader topics
- Neoplasms, Germ Cell and Embryonal; Neoplasms, Nerve Tissue
- Narrower topics
- Craniopharyngioma; Neoplasms, Neuroepithelial; Neuroectodermal Tumor, Melanotic; Neuroendocrine Tumors
Research landscape
PubMed indexes 373,877 records tagged with the MeSH heading “Neuroectodermal Tumors” (counts retrieved 2026-10-29). 79,623 of them (21.3%) were published from 2020 onward, and the busiest period so far is through 1999 with 120,056 records.
Reviews account for 44,533 records (11.9%) and meta-analyses for 2,237. Randomized controlled trials number 2,613 (0.7%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 120,056 |
| 2000-2009 | 68,132 |
| 2010-2019 | 106,066 |
| 2020 onward | 79,623 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 44,533 | 11.9% |
| Meta-analyses | 2,237 | 0.6% |
| Randomized controlled trials | 2,613 | 0.7% |
Method: PubMed query "Neuroectodermal Tumors"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in cancer and oncology
Cancer research spans very different kinds of evidence. Laboratory studies in cell lines and animal models reveal mechanisms but often do not translate to patients. Early-phase trials mainly test safety and dosing, while phase 3 randomized trials and their meta-analyses are the usual basis for treatment conclusions. Outcomes also differ in meaning: tumour shrinkage, progression-free survival and overall survival are not interchangeable, and screening studies can be distorted by lead-time and overdiagnosis. When reading a result, check the cancer type and stage studied, the comparison treatment, and which outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| NRF2 activation is required for chemotherapy resistance acquisition in medulloblastoma via metabolic and redox adaptation | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42704985 · DOI · PMC13579287 |
| Divergent medulloblastoma chromatin states disclose KDM2B as a selective dependency | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42786297 · DOI · PMC13649585 |
| Tunneling nanotubes regulate mitochondrial homeostasis between glioblastoma and astrocytes, and between tumor cells in vivo | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42744791 · DOI · PMC13578765 |
| Targeting USP14 sensitizes glioma to radiotherapy through exacerbated reactive oxygen species accumulation | 2027 | Research article Design not recorded in structured metadata | 0 | cc by PMID 42734450 · DOI · PMC13667373 |
NRF2 activation is required for chemotherapy resistance acquisition in medulloblastoma via metabolic and redox adaptation [1]
Abstract reading summary — source excerpts
- Opening excerpt
- This study explores the pivotal role of NRF2 signaling in conferring resistance to chemotherapy and ferroptosis in medulloblastoma (MB), a highly malignant pediatric brain tumor.
- Closing excerpt
- Targeting NRF2 signaling may provide a novel approach to overcome therapy resistance and improve treatment outcomes for patients with this challenging cancer.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (263 words)
This study explores the pivotal role of NRF2 signaling in conferring resistance to chemotherapy and ferroptosis in medulloblastoma (MB), a highly malignant pediatric brain tumor. Using newly developed in vitro models of MB cells, resistant to standard chemotherapeutics (vincistine, etoposide, cisplatin, and cyclophosphamide), we observed that chemotolerant cells exhibit an enhanced antioxidant response. Specifically, we found higher levels of glutathione, compared to sensitive cells, and increased thioredoxin reductase activity, both key components in maintaining redox homeostasis. Furthermore, we identified a metabolic shift in resistant cells, marked by increased flux through the pentose phosphate pathway (PPP), which boosts NADPH production and supports the antioxidant defense mechanisms. This adaptive antioxidant response is largely mediated by hyperactivation of the NRF2 transcription factor and the consequent upregulation of a set of antioxidant genes, thus effectively reducing intracellular reactive oxygen species (ROS) levels and enhancing cells' ability to tolerate oxidative stress. Intriguingly, our results suggest that NRF2 activation not only supports the acquisition of chemotherapy resistance but also confers protection against ferroptosis induction. Indeed, resistant cells upregulate iron sequestration proteins and ferroptosis-suppressing genes, directly controlled by NRF2, thereby reducing vulnerability to lipid peroxidation-induced cell death. Inhibition of NRF2 in resistant cells increased their sensitivity to both chemotherapy and ferroptosis inducers and, more interestingly, its knockdown prevented sensitive cells from acquiring resistance. Overall, our study underscores the crucial role of NRF2-controlled redox homeostasis in mediating resistance mechanisms in MB, highlighting the therapeutic potential of targeting this pathway. Targeting NRF2 signaling may provide a novel approach to overcome therapy resistance and improve treatment outcomes for patients with this challenging cancer.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42704985 · DOI · PMC13579287
Divergent medulloblastoma chromatin states disclose KDM2B as a selective dependency [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Medulloblastoma is a biologically heterogeneous childhood cerebellar tumor harboring frequent chromatin-modifying gene alterations.
- Closing excerpt
- Collectively, we provide foundational insights into an epigenetic basis of medulloblastoma, nominating KDM2B as a selective dependency in high-risk subgroups that warrants consideration as a candidate therapeutic target.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (147 words)
Medulloblastoma is a biologically heterogeneous childhood cerebellar tumor harboring frequent chromatin-modifying gene alterations. How these alterations promote transcriptional programs governing malignancy remains poorly defined. To address this knowledge gap, we evaluated chromatin states across medulloblastoma subgroups by multi-modal integration of histone modifications with mutational, DNA methylation and transcriptomic profiles. A bivalent/poised enhancer (EnhBiv) state was specifically enriched at the promoters of neurodevelopmental genes in Group 3/4 medulloblastoma. Integrative bioinformatics coupled with chromatin occupancy studies identified aberrant KDM2B binding at EnhBiv-enriched promoters. CRISPR-mediated knockout or acute protein degradation of KDM2B selectively suppressed the growth of medulloblastoma models in vitro and in vivo. Mechanistically, KDM2B promotes sequential recruitment of Polycomb repressive complexes (PRC1/PRC2) and EnhBiv chromatin, thereby repressing neuronal differentiation programs. Collectively, we provide foundational insights into an epigenetic basis of medulloblastoma, nominating KDM2B as a selective dependency in high-risk subgroups that warrants consideration as a candidate therapeutic target.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42786297 · DOI · PMC13649585
Tunneling nanotubes regulate mitochondrial homeostasis between glioblastoma and astrocytes, and between tumor cells in vivo [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Tumor progression is driven by cancer cells' ability to establish a cellular network through tunneling nanotube-like connections (TNTs), which enable mitochondrial exchange both within the tumor cells and with the tumor microenvironment (TME).
- Closing excerpt
- These findings reveal a potential mechanism of tumor adaptation and highlight TNTs as promising therapeutic targets.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (150 words)
Tumor progression is driven by cancer cells' ability to establish a cellular network through tunneling nanotube-like connections (TNTs), which enable mitochondrial exchange both within the tumor cells and with the tumor microenvironment (TME). However, the functional consequences of mitochondrial transfer between tumor and non-tumor cells, and its occurrence in vivo, remain poorly understood. Here we show bidirectional mitochondrial transfer between Glioblastoma (GBM) cells and non-tumoral astrocytes (AS). We report that transfer of damaged mitochondria from GBM cells to AS is associated with activation of mitophagy in recipient cells, while astrocyte-derived mitochondria to GBM cells correlates with changes in mitochondrial activity and metabolic readouts. Furthermore, intravital subcellular microscopy (ISMic) in a live animal model allows the visualization of TNT connections with characteristics similar to those observed in vitro and supported TNT-mediated mitochondrial transfer in vivo. These findings reveal a potential mechanism of tumor adaptation and highlight TNTs as promising therapeutic targets.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42744791 · DOI · PMC13578765
Targeting USP14 sensitizes glioma to radiotherapy through exacerbated reactive oxygen species accumulation [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Radiotherapy is one of the most effective treatments for glioma, but therapeutic efficacy is strongly limited due to intrinsic radioresistance, which is closely linked to reactive oxygen species.
- Closing excerpt
- In summary, we reveal a new regulatory axis by which USP14 governs glioma radiosensitivity through reactive oxygen species-mediated DNA damage and apoptosis, providing a promising therapeutic target and strategy for reversing clinical radioresistance.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (195 words)
Radiotherapy is one of the most effective treatments for glioma, but therapeutic efficacy is strongly limited due to intrinsic radioresistance, which is closely linked to reactive oxygen species. This research was designed to elucidate the role and underlying mechanisms of the deubiquitinase ubiquitin-specific protease 14 (USP14) in reactive oxygen species Accumulation and radioresistance of glioma. Bioinformatics analysis demonstrated that upregulation of USP14 was associated with tumor progression, high levels of USP14 in glioma patients were correlated with a significantly poorer prognosis. Cytological experimental results demonstrated that radiotherapy could induce increased USP14 expression. Inhibition of USP14 disrupted intracellular protein homeostasis, leading to upregulation of endoplasmic reticulum stress-related proteins thereby exacerbating endoplasmic reticulum stress. This stress response further induced substantial reactive oxygen species generation and DNA damage accumulation, ultimately synergistically enhancing the tumoricidal effect of radiotherapy. In vivo, the combined application of b-AP15 (a USP14 inhibitor) and radiotherapy elicited potent antitumor effects, marked by significant suppression of tumor growth and increased apoptotic cell death. In summary, we reveal a new regulatory axis by which USP14 governs glioma radiosensitivity through reactive oxygen species-mediated DNA damage and apoptosis, providing a promising therapeutic target and strategy for reversing clinical radioresistance.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42734450 · DOI · PMC13667373
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Prognostic value of inflammatory markers NLR, PLR, LMR, dNLR, ANC in melanoma patients treated with immune checkpoint inhibitors: a meta-analysis and systematic review [5]
- Research article Pituitary neuroendocrine tumors with PIT1/SF1 co-expression show distinct clinicopathological and molecular features [6]
- Research article Efficacy of TIL therapy in advanced cutaneous melanoma in the current immuno-oncology era: updated systematic review and meta-analysis [7]
- Research article Skin Cancer Diagnosis by Lesion, Physician, and Examination Type: A Systematic Review and Meta-Analysis [8]
- Research article The Prognostic Significance of Epidermal Growth Factor Receptor Amplification and Epidermal Growth Factor Receptor Variant III Mutation in Glioblastoma: A Systematic Review and Meta-Analysis with Implications for Targeted Therapy [9]
- Research article Repeat stereotactic radiosurgery in vestibular schwannoma patients: A systematic review and meta-analysis [10]
References
- Manfreda L, Rruga F, Zanolli A, Marzullo BP, Vettore L, Mozzo M, et al.. NRF2 activation is required for chemotherapy resistance acquisition in medulloblastoma via metabolic and redox adaptation. . 2026. PMID 42704985 · DOI · PMC13579287
- Tao R, Erkek-Ozhan S, Xu B, Matsui Y, Mittal P, Smith KS, et al.. Divergent medulloblastoma chromatin states disclose KDM2B as a selective dependency. . 2026. PMID 42786297 · DOI · PMC13649585
- Saenz-de-Santa-Maria I, Pepe A, Tinevez JY, Brou C, Vitrenko Y, Cokelaer T, et al.. Tunneling nanotubes regulate mitochondrial homeostasis between glioblastoma and astrocytes, and between tumor cells in vivo. . 2026. PMID 42744791 · DOI · PMC13578765
- Liu X, Shen L, Lu Y, Wang Z, Yuan S, Gu H, et al.. Targeting USP14 sensitizes glioma to radiotherapy through exacerbated reactive oxygen species accumulation. . 2027. PMID 42734450 · DOI · PMC13667373
- Ou Y, Liang S, Gao Q, Shang Y, Liang J, Zhang W, et al.. Prognostic value of inflammatory markers NLR, PLR, LMR, dNLR, ANC in melanoma patients treated with immune checkpoint inhibitors: a meta-analysis and systematic review. Front Immunol. 2024. PMID 39493767 · DOI · PMC11527641
- Dottermusch M, Ryba A, Ricklefs FL, Flitsch J, Schmid S, Glatzel M, et al.. Pituitary neuroendocrine tumors with PIT1/SF1 co-expression show distinct clinicopathological and molecular features. Acta Neuropathol. 2024. PMID 38228887 · DOI · PMC10791732
- Martín-Lluesma S, Svane IM, Dafni U, Vervita K, Karlis D, Dimopoulou G, et al.. Efficacy of TIL therapy in advanced cutaneous melanoma in the current immuno-oncology era: updated systematic review and meta-analysis. Ann Oncol. 2024. PMID 39053767 · DOI
- Chen JY, Fernandez K, Fadadu RP, Reddy R, Kim MO, Tan J, et al.. Skin Cancer Diagnosis by Lesion, Physician, and Examination Type: A Systematic Review and Meta-Analysis. JAMA Dermatol. 2025. PMID 39535756 · DOI · PMC11561728
- Zhu F, Qiu J, Ye H, Su W, Wang R, Fu Y. The Prognostic Significance of Epidermal Growth Factor Receptor Amplification and Epidermal Growth Factor Receptor Variant III Mutation in Glioblastoma: A Systematic Review and Meta-Analysis with Implications for Targeted Therapy. Int J Mol Sci. 2025. PMID 40331985 · DOI · PMC12027172
- Hajikarimloo B, Habibi MA, Sabbagh Alvani M, Zare AH, Tos SM, Sheehan JP. Repeat stereotactic radiosurgery in vestibular schwannoma patients: A systematic review and meta-analysis. J Clin Neurosci. 2024. PMID 39504737 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.