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 (576 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
A malignant neoplasm derived from cells that are capable of forming melanin, which may occur in the skin of any part of the body, in the eye, or, rarely, in the mucous membranes of the genitalia, anus, oral cavity, or other sites. It occurs mostly in adults and may originate de novo or from a pigmented nevus or malignant lentigo. Melanomas frequently metastasize widely, and the regional lymph nodes, liver, lungs, and brain are likely to be involved. The incidence of malignant skin melanomas is rising rapidly in all parts of the world. (Stedman, 25th ed; from Rook et al., Textbook of Dermatology, 4th ed, p2445)
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: Melanomas; Malignant Melanoma; Malignant Melanomas; Melanoma, Malignant; Melanomas, Malignant.
Where it fits in the MeSH classification
- Broader topics
- Neuroendocrine Tumors; Nevi and Melanomas; Skin Neoplasms
- Narrower topics
- Cutaneous Malignant Melanoma; Hutchinson's Melanotic Freckle; Melanoma, Amelanotic; Melanoma, Experimental; Uveal Melanoma
Research landscape
PubMed indexes 120,128 records tagged with the MeSH heading “Melanoma” (counts retrieved 2026-10-29). 24,717 of them (20.6%) were published from 2020 onward, and the busiest period so far is through 1999 with 38,103 records.
Reviews account for 13,872 records (11.5%) and meta-analyses for 720. Randomized controlled trials number 1,361 (1.1%) 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 | 38,103 |
| 2000-2009 | 22,461 |
| 2010-2019 | 34,847 |
| 2020 onward | 24,717 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 13,872 | 11.5% |
| Meta-analyses | 720 | 0.6% |
| Randomized controlled trials | 1,361 | 1.1% |
Method: PubMed query "Melanoma"[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 |
|---|---|---|---|---|
| CD44 restricts EGFR mobility to polarize cytoskeletal signalling modules driving bleb-based migration | 2026 | Research article Design not recorded in structured metadata | 4 | cc by PMID 42410113 · DOI · PMC13364714 |
| Efficacy and safety evaluation of gilvetmab in dogs with melanoma and mast cell tumor | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 42247661 · DOI · PMC13240851 |
| 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 |
CD44 restricts EGFR mobility to polarize cytoskeletal signalling modules driving bleb-based migration [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Cells under high confinement migrate efficiently in low-adhesion environments by forming stable, polarized, hydrostatic pressure-driven leader blebs.
- Closing excerpt
- Together, these findings define the biophysical and molecular mechanisms that underlie polarity in bleb-based migration and highlight how alternative spatial organization of signalling modules supports distinct migration modes in different microenvironments.
- 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 (179 words)
Cells under high confinement migrate efficiently in low-adhesion environments by forming stable, polarized, hydrostatic pressure-driven leader blebs. Here we investigated the basis of polarized bleb morphology in metastatic melanoma cells migrating under low-adhesive and highly confined microenvironments. Using high-resolution live imaging, molecular perturbations and biosensors, we show that EGF signalling through PI3K stabilizes and maintains polarized leader blebs. EGFR and PI3K activities form a gradient within leader blebs that decreases from rear to front, promoting phosphatidylinositol 3,4,5-trisphosphate and Rac1-GTP accumulation at the bleb rear, whereas phosphatidylinositol 4,5-bisphosphate and RhoA-GTP concentrate at the bleb tip, the inverse of the organization observed in integrin-dependent mesenchymal migration. Optogenetic disruption of this gradient triggers bleb retraction, underscoring its functional importance. Mathematical modelling and experiments identified a mechanism whereby during bleb initiation, CD44 and ERM proteins restrict EGFR mobility within a membrane-apposed cortical actin meshwork at the bleb rear, establishing the EGFR-PI3K-Rac gradient. Together, these findings define the biophysical and molecular mechanisms that underlie polarity in bleb-based migration and highlight how alternative spatial organization of signalling modules supports distinct migration modes in different microenvironments.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42410113 · DOI · PMC13364714
Efficacy and safety evaluation of gilvetmab in dogs with melanoma and mast cell tumor [2]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundImmune checkpoint inhibitors (ICIs) have transformed oncology in human medicine, providing clinical benefit in a broad spectrum of cancers.
- Closing excerpt
- Conclusions and clinical importanceGilvetmab has a reasonable expectation of efficacy and an acceptable preliminary safety profile in dogs with MCT stages I-III and melanoma stages II and III.
- 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 (228 words)
BackgroundImmune checkpoint inhibitors (ICIs) have transformed oncology in human medicine, providing clinical benefit in a broad spectrum of cancers. Widely available ICIs for dogs are lacking.Hypothesis/objectivesEvaluate efficacy and safety of gilvetmab, a caninized anti-PD-1 monoclonal antibody.AnimalsFifty-one client-owned dogs were evaluated, 25 with stages II-III melanoma and 26 with stages I-III mast cell tumor (MCT). Fifteen dogs with stages III-V lymphoma were also evaluated.MethodsMulti-institutional, open-label study. Enrolled dogs were treated with gilvetmab IV at 6 mg/kg q28d or 10 mg/kg q14d; 8 dogs receiving the lower dosage underwent dose escalation with their owners' consent. Safety was evaluated by physical examinations, laboratory testing, and clinical observations made by veterinarians or the dogs' owners. Efficacy was assessed by objective response rate (ORR) and time to progression (TTP) using cRECIST v1.0 and lymphoma response criteria.ResultsFor melanoma, the ORR was 20% (95% confidence interval [CI], 7%-41%) and median TTP was 56 days. For MCT, the ORR was 46% (95% CI, 27%-67%) and median TTP was not reached. No objective responses were observed in dogs with lymphoma. Serious adverse events of anaphylaxis, hypotension, or tumor hemorrhage occurred in 3 dogs (3/51, 5.9%). Tumor enlargement before regression, consistent with possible pseudoprogression, was observed in 2 dogs with melanoma.Conclusions and clinical importanceGilvetmab has a reasonable expectation of efficacy and an acceptable preliminary safety profile in dogs with MCT stages I-III and melanoma stages II and III.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42247661 · DOI · PMC13240851
Selective mRNA translation determines adaptative mutability of melanoma cells to anti-BRAF/MEK combination therapy [3]
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
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 Cutaneous melanoma attributable to sunbed use: systematic review and meta-analysis [5]
- Research article Overall survival after treatment for metastatic uveal melanoma: a systematic review and meta-analysis [6]
- Research article Genome-wide association meta-analyses combining multiple risk phenotypes provide insights into the genetic architecture of cutaneous melanoma susceptibility [7]
- Research article Endometriosis and cancer: a systematic review and meta-analysis [8]
- Research article A meta-analysis of nevus-associated melanoma: Prevalence and practical implications [9]
References
- Jha A, Chandra A, Farahani PE, Toettcher JE, Pasapera AM, Haugh JM, et al.. CD44 restricts EGFR mobility to polarize cytoskeletal signalling modules driving bleb-based migration. . 2026. PMID 42410113 · DOI · PMC13364714
- Chon E, Morsey M, Katz T, Yamada K, Bailey D, Bergman PJ, et al.. Efficacy and safety evaluation of gilvetmab in dogs with melanoma and mast cell tumor. . 2026. PMID 42247661 · DOI · PMC13240851
- 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
- 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
- Boniol M, Autier P, Boyle P, Gandini S. Cutaneous melanoma attributable to sunbed use: systematic review and meta-analysis. BMJ. 2012. PMID 22833605 · DOI · PMC3404185
- Rantala ES, Hernberg M, Kivelä TT. Overall survival after treatment for metastatic uveal melanoma: a systematic review and meta-analysis. Melanoma Res. 2019. PMID 30664106 · DOI · PMC6887637
- Landi MT, Bishop DT, MacGregor S, Machiela MJ, Stratigos AJ, Ghiorzo P, et al.. Genome-wide association meta-analyses combining multiple risk phenotypes provide insights into the genetic architecture of cutaneous melanoma susceptibility. Nat Genet. 2020. PMID 32341527 · DOI · PMC7255059
- 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
- Pampena R, Kyrgidis A, Lallas A, Moscarella E, Argenziano G, Longo C. A meta-analysis of nevus-associated melanoma: Prevalence and practical implications. J Am Acad Dermatol. 2017. PMID 28864306 · 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.
See how EvidenceLib is built. Spotted an error? Email support@evidencehelix.com.
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.