Evidence map›Paper›PMID 26300491›Full record

ReviewPigment cell & melanoma research2015

Genetics of melanocytic nevi.

Mi Ryung Roh, Philip Eliades, Sameer Gupta, Hensin Tsao

Open access · bronzeAbstract readReview
In one paragraph

Review in Pigment cell & melanoma research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
6.6field-weighted citation impact, top 2% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

66 citing papers in PubMed, 176 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
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  6. Article
  7. Review
  8. Article
  9. Crosstalk in Skin: Loss of Desmoglein 1 in Keratinocytes Inhibits BRAFThe Journal of investigative dermatology · 2025
    Article
  10. An overview of benefits and risks of chronic melanocortin-1 receptor activation.Journal of the European Academy of Dermatology and Venereology : JEADV · 2025
    Review
  11. Melanocytoma of the eyelid: Case report and introduction of new nomenclature.American journal of ophthalmology case reports · 2024
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

6 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 2 countries.

Mi Ryung RohWellman Center for Photomedicine, Department of Dermatology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Philip EliadesWellman Center for Photomedicine, Department of Dermatology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Sameer GuptaWellman Center for Photomedicine, Department of Dermatology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Hensin TsaoWellman Center for Photomedicine, Department of Dermatology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Harvard University · USTufts University · USYonsei University · KR

Funding

Molecular Risk Assessment in Hereditary MelanomaK24CA149202 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI TSAO, HENSIN · 2010 to 2019
$1.9M
NCI NIH HHS K24 CA149202NCI NIH HHS K24CA149202
6 · The paper itself

Abstract

Melanocytic nevi are a benign clonal proliferation of cells expressing the melanocytic phenotype, with heterogeneous clinical and molecular characteristics. In this review, we discuss the genetics of nevi by salient nevi subtypes: congenital melanocytic nevi, acquired melanocytic nevi, blue nevi, and Spitz nevi. While the molecular etiology of nevi has been less thoroughly studied than melanoma, it is clear that nevi and melanoma share common driver mutations. Acquired melanocytic nevi harbor oncogenic mutations in BRAF, which is the predominant oncogene associated with melanoma. Congenital melanocytic nevi and blue nevi frequently harbor NRAS mutations and GNAQ mutations, respectively, while Spitz and atypical Spitz tumors often exhibit HRAS and kinase rearrangements. These initial 'driver' mutations are thought to trigger the establishment of benign nevi. After this initial phase of the cell proliferation, a senescence program is executed, causing termination of nevi growth. Only upon the emergence of additional tumorigenic alterations, which may provide an escape from oncogene-induced senescence, can malignant progression occur. Here, we review the current literature on the pathobiology and genetics of nevi in the hope that additional studies of nevi promise to inform our understanding of the transition from benign neoplasm to malignancy.

Indexed as

Genetic Predisposition to DiseaseCarcinogenesisHumansNevus, PigmentedSkin Neoplasmsacquired melanocytic neviblue nevicongenital melanocytic nevigeneticsSpitz nevi

Identifiers

PMID26300491
PMCPMC4609613
OpenAlexW2134570345

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.