Evidence map›Paper›PMID 40459282›Full record

ArticleJournal of cutaneous pathology2025

Large Congenital Melanocytic Nevus With LMNA::NTRK1 Fusion: Expanding Targeted Therapy Options for Congenital Nevi and Melanoma.

Akanksha Nagarkar, Jackson Turbeville, Molly A Hinshaw, Philip E LeBoit, Jeffrey Gagan, Mark Raffeld, Kenneth Aldape, Niharika Shah, Frederic G Barr, Liqiang Xi and 7 more

Abstract readCase Reports
In one paragraph

Article in Journal of cutaneous pathology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
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

17 authors.

Akanksha NagarkarDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, Maryland, United States.
Jackson TurbevilleDepartment of Dermatology, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, United States.
Molly A HinshawDepartment of Dermatology, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, United States.ORCID https://orcid.org/0000-0002-9440-7762
Philip E LeBoitDermatology and Pathology, Helen Diller Family Cancer Center, University of California, San Francisco, California, United States.
Jeffrey GaganLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States.
Mark RaffeldLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States.
Kenneth AldapeLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States.
Niharika ShahLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States.
Frederic G BarrLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States.
Liqiang XiLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States.
Ina LeeLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States.
Christina K FerroneLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States.
Svetlana D PackLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States.
Rosandra KaplanPediatric Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States.
Mary Frances Wedekind MalonePediatric Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States.
Marielle YoheLaboratory of Cell and Developmental Signaling, National Cancer Institute, National Institutes of Health, Frederick, Maryland, United States.
Michael R SargenDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, Maryland, United States.

Funding

Intramural NIH HHS Z99 CA999999NCI NIH HHSNIH HHS
6 · The paper itself

Abstract

Large congenital melanocytic nevi/nevus (LCMN) are caused by genetic events that activate the mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase (ERK) pathway. Individuals with LCMN are prone to developing aggressive melanomas during childhood. Targeted therapies are needed to treat this form of melanoma and manage LCMN symptoms such as pruritus and pain, which significantly impact quality of life. Here, we present the first case of an LCMN with an NTRK fusion driver event. The patient presented with an atypical proliferative nodule arising in the background nevus. RNA sequencing of the proliferative nodule with background nevus identified a pathogenic LMNA::NTRK1 fusion. The fusion resulted in constitutive expression of TrkA, demonstrated by strong cytoplasmic pan-TRK staining, along with activation of the MAPK/ERK pathway, as indicated by positive nuclear and cytoplasmic staining for phosphorylated ERK. The background nevus beneath the proliferative nodule also expressed pan-TRK and phosphorylated ERK, suggesting that the NTRK1 fusion occurred prior to the formation of the proliferative nodule. This case broadens the spectrum of driver events for LCMN and suggests that screening for TRK fusions in LCMN should be considered when systemic therapy is being considered for melanoma or symptom management.

Indexed as

Lamin Type ANevus, PigmentedOncogene Proteins, FusionReceptor, trkASkin NeoplasmsHumansMAP Kinase Signaling SystemLamin Type ALMNA protein, humanNTRK1 protein, humanOncogene Proteins, FusionReceptor, trkAcongenital melanocytic nevimelanomanevusNTRK fusionproliferative nodule

Identifiers

PMID40459282
PMCPMC12227274

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.