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: 3 complete abstracts (567 words), 9 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
Tumors whose cells possess secretory granules and originate from the neuroectoderm, i.e., the cells of the ectoblast or epiblast that program the neuroendocrine system. Common properties across most neuroendocrine tumors include ectopic hormone production (often via apud cells), the presence of tumor-associated antigens, and isozyme composition.
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: Neuroendocrine Tumor; Tumor, Neuroendocrine; Tumors, Neuroendocrine.
Where it fits in the MeSH classification
- Broader topics
- Neuroectodermal Tumors
- Narrower topics
- Adenoma, Acidophil; Adenoma, Basophil; Adenoma, Chromophobe; Apudoma; Carcinoid Tumor; Carcinoma, Neuroendocrine; Melanoma; Neurilemmoma; Paraganglioma
Related concepts
- Apud Cells
Research landscape
PubMed indexes 211,096 records tagged with the MeSH heading “Neuroendocrine Tumors” (counts retrieved 2026-10-29). 41,054 of them (19.4%) were published from 2020 onward, and the busiest period so far is through 1999 with 74,314 records.
Reviews account for 26,948 records (12.8%) and meta-analyses for 1,185. Randomized controlled trials number 1,653 (0.8%) 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 | 74,314 |
| 2000-2009 | 38,122 |
| 2010-2019 | 57,606 |
| 2020 onward | 41,054 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 26,948 | 12.8% |
| Meta-analyses | 1,185 | 0.6% |
| Randomized controlled trials | 1,653 | 0.8% |
Method: PubMed query "Neuroendocrine 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 |
|---|---|---|---|---|
| Selective mRNA translation determines adaptative mutability of melanoma cells to anti-BRAF/MEK combination therapy | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42477455 · DOI · PMC13470486 |
| Long-read sequencing of single cell-derived melanoma sublines reveals divergent and parallel genomic and epigenomic evolutionary trajectories | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42463712 · DOI · PMC13493970 |
| PLA2G2D in tumour-draining lymph nodes regulates anti-tumour immunity | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42717091 · DOI · PMC13645638 |
Selective mRNA translation determines adaptative mutability of melanoma cells to anti-BRAF/MEK combination therapy [1]
Abstract reading summary — source excerpts
- Opening excerpt
- During their inevitable evolution towards acquired resistance to anti-cancer targeted therapies, cancer cells adopt distinct gene expression profiles that allow them to transiently adapt to and tolerate the treatment.
- Closing excerpt
- Our results demonstrate that a standard-of-care therapy for melanoma, by engaging non-genetic adaptation driven at the translational level, contributes to the evolution of drug-tolerant melanoma cells toward acquired resistance.
- 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 (169 words)
During their inevitable evolution towards acquired resistance to anti-cancer targeted therapies, cancer cells adopt distinct gene expression profiles that allow them to transiently adapt to and tolerate the treatment. Cancer cells surviving therapy can increase their mutation rate, enhancing the likelihood of acquiring resistance-conferring mutations and evolving into resistant cells. Here we show that translational control mediates the adaptive mutability of melanoma drug-tolerant cells by regulating the translation of the error-prone non-homologous end joining (NHEJ) component 53BP1. The specific inhibition of 5'UTR-driven 53BP1 mRNA translation was sufficient to impair NHEJ and mutability. We found that the eIF4A RNA helicase, regulates 53BP1 mRNA translation. Consequently, targeting the eIF4A with two small molecule inhibitors significantly delays the acquisition of resistance to combination of BRAF and MEK inhibitors in BRAFV600-mutant melanoma xenograft models and cell lines by reducing the mutability of drug-tolerant cells. Our results demonstrate that a standard-of-care therapy for melanoma, by engaging non-genetic adaptation driven at the translational level, contributes to the evolution of drug-tolerant melanoma cells toward acquired resistance.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42477455 · DOI · PMC13470486
Long-read sequencing of single cell-derived melanoma sublines reveals divergent and parallel genomic and epigenomic evolutionary trajectories [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Tumor evolution is driven by various mutational processes, ranging from single-nucleotide variants (SNVs) to large structural variants (SVs) to dynamic shifts in DNA methylation.
- Closing excerpt
- We also show our set of phylogeny-constrained variant calls along with openly released sequencing data can be a valuable resource for the development and benchmarking of computational methods.
- 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 (182 words)
Tumor evolution is driven by various mutational processes, ranging from single-nucleotide variants (SNVs) to large structural variants (SVs) to dynamic shifts in DNA methylation. Current short-read sequencing methods struggle to accurately capture the full spectrum of these genomic and epigenomic alterations due to inherent technical limitations. To overcome that, here we introduce an approach to identify and analyze the genomic and epigenetic events in different stages of tumoral evolution from long-read sequencing of single-cell derived sublines. We then use it to profile 23 sublines of a mouse cutaneous melanoma cell line, characterized with distinct growth phenotypes and treatment responses. We develop a computational framework for harmonization and joint analysis of different variant types in the evolutionary context. Uniquely, our framework enables detection of recurrent amplifications of putative driver genes, generated by independent SVs across different lineages, suggesting parallel evolution. In addition, our approach revealed gradual and lineage-specific methylation changes associated with aggressive clonal phenotypes. We also show our set of phylogeny-constrained variant calls along with openly released sequencing data can be a valuable resource for the development and benchmarking of computational methods.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42463712 · DOI · PMC13493970
PLA2G2D in tumour-draining lymph nodes regulates anti-tumour immunity [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Systemic anti-tumour immunity results from T cell priming in tumour-draining lymph nodes (TDLNs)1-4.
- Closing excerpt
- Collectively, our in-depth spatial profiling identifies PLA2G2D as a TDLN-centred targetable immune checkpoint for cancer immunotherapy.
- 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 (216 words)
Systemic anti-tumour immunity results from T cell priming in tumour-draining lymph nodes (TDLNs)1-4. Although the suppression of T cells in tumours is well characterized5-8, whether this occurs in TDLNs-and if so, through which mechanisms-remains poorly understood. Here, using imaging mass cytometry of TDLNs from patients with melanoma, we identify a spatial neighbourhood in the TDLN paracortex that is linked to the development of distant metastases. Targeted spatial transcriptomics of cells inside this neighbourhood revealed activated CD8+ T cells engaging with myeloid cells that expressed high levels of the immunosuppressive secretory phospholipase PLA2G2D. PLA2G2D+ myeloid cells were substantially more abundant in TDLNs than they were in primary tumours or metastases. Genetic loss-of-function or antibody-mediated inhibition of PLA2G2D reduced tumour growth markedly, and single-cell transcriptomics in melanoma-bearing mice revealed that expression of Pla2g2d is confined to lymph-node macrophages. Mechanistically, PLA2G2D directly suppressed the early proliferation of T cells in vitro, and inhibiting PLA2G2D resulted in an expansion of tumour-specific T cells in TDLNs, leading to an increase in these T cells in the circulation and subsequently in tumours. Notably, PLA2G2D and PD-1 act as non-redundant immune checkpoints, with combination treatment showing additive or synergistic efficacy in humanized mice treated with human-specific antibodies. Collectively, our in-depth spatial profiling identifies PLA2G2D as a TDLN-centred targetable immune checkpoint for cancer immunotherapy.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42717091 · DOI · PMC13645638
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 Intestinal microbiota signatures of clinical response and immune-related adverse events in melanoma patients treated with anti-PD-1 [4]
- Research article Endometriosis and cancer: a systematic review and meta-analysis [5]
- Research article Ki-67 assessment of pancreatic neuroendocrine neoplasms: Systematic review and meta-analysis of manual vs. digital pathology scoring [6]
- Research article Efficacy and Safety of Endoscopic Ultrasound-Guided Radiofrequency Ablation for Pancreatic Neuroendocrine Tumors: A Systematic Review and Metanalysis [7]
- Research article Reliability of grading preoperative pancreatic neuroendocrine tumors on EUS specimens: a systematic review with meta-analysis of aggregate and individual data [8]
- 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 [9]
References
- Fabbri L, Lagadec L, Guérin E, Lecourt H, Baille D, Besse L, et al.. Selective mRNA translation determines adaptative mutability of melanoma cells to anti-BRAF/MEK combination therapy. . 2026. PMID 42477455 · DOI · PMC13470486
- Liu Y, Goretsky A, Keskus AG, Malikic S, Ahmad T, Gertz EM, et al.. Long-read sequencing of single cell-derived melanoma sublines reveals divergent and parallel genomic and epigenomic evolutionary trajectories. . 2026. PMID 42463712 · DOI · PMC13493970
- van Krimpen A, Huang J, Eterman M, Gerretsen V, Umetani M, Janssen JC, et al.. PLA2G2D in tumour-draining lymph nodes regulates anti-tumour immunity. . 2026. PMID 42717091 · DOI · PMC13645638
- McCulloch JA, Davar D, Rodrigues RR, Badger JH, Fang JR, Cole AM, et al.. Intestinal microbiota signatures of clinical response and immune-related adverse events in melanoma patients treated with anti-PD-1. Nat Med. 2022. PMID 35228752 · DOI · PMC10246505
- Kvaskoff M, Mahamat-Saleh Y, Farland LV, Shigesi N, Terry KL, Harris HR, et al.. Endometriosis and cancer: a systematic review and meta-analysis. Hum Reprod Update. 2021. PMID 33202017 · DOI
- Luchini C, Pantanowitz L, Adsay V, Asa SL, Antonini P, Girolami I, et al.. Ki-67 assessment of pancreatic neuroendocrine neoplasms: Systematic review and meta-analysis of manual vs. digital pathology scoring. Mod Pathol. 2022. PMID 35249100 · DOI · PMC9174054
- Armellini E, Facciorusso A, Crinò SF. Efficacy and Safety of Endoscopic Ultrasound-Guided Radiofrequency Ablation for Pancreatic Neuroendocrine Tumors: A Systematic Review and Metanalysis. Medicina (Kaunas). 2023. PMID 36837560 · DOI · PMC9963038
- Tacelli M, Bina N, Crinò SF, Facciorusso A, Celsa C, Vanni AS, et al.. Reliability of grading preoperative pancreatic neuroendocrine tumors on EUS specimens: a systematic review with meta-analysis of aggregate and individual data. Gastrointest Endosc. 2022. PMID 35863518 · DOI
- 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
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.