Evidence map›Paper›PMID 41673532›Full record

ArticlePigment cell & melanoma research2026

Rare Germline Variants in CDKN2A-Negative Children and Adolescents With Cutaneous Melanoma.

Peter A Johansson, Jane M Palmer, Linh T Bui-Raborn, Mai Xu, Kristine M Jones, Herbert Higson, Jia Liu, Kelly M Brooks, Antonia L Pritchard, Nicholas K Hayward and 1 more

Abstract read
In one paragraph

Article in Pigment cell & melanoma research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

11 authors.

Peter A JohanssonOncogenomics Group, QIMR Berghofer, Brisbane, Queensland, Australia.ORCID 0000-0001-7015-5452
Jane M PalmerOncogenomics Group, QIMR Berghofer, Brisbane, Queensland, Australia.
Linh T Bui-RabornDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Mai XuDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Kristine M JonesDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Herbert HigsonDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Jia LiuDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Kelly M BrooksOncogenomics Group, QIMR Berghofer, Brisbane, Queensland, Australia.
Antonia L PritchardOncogenomics Group, QIMR Berghofer, Brisbane, Queensland, Australia.
Nicholas K HaywardOncogenomics Group, QIMR Berghofer, Brisbane, Queensland, Australia.
Kevin M BrownDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.

Funding

Buckoff MelanomaNational Health and Medical Research Council APP1195581NCI NIH HHS
6 · The paper itself

Abstract

Cutaneous melanoma is a complex disease influenced by both environmental and genetic factors. Inherited susceptibility plays a significant role, involving a combination of high-, intermediate- and low-penetrance genes. Melanoma in children and adolescents has been speculated to have a stronger genetic component due to the early onset. This study investigates germline variants in early-onset melanoma through exome sequencing of 154 patients in Australia diagnosed with cutaneous melanoma before the age of 20. Potentially pathogenic variants in shelterin complex genes were identified in 3% of the cases, consistent with a role for telomere dysregulation in early-onset melanoma. MC1R R-alleles, associated with red hair, fair skin and increased melanoma risk, were less frequent than in adult cases (0.46 vs. 0.64). Pathogenic germline variants in pigmentation genes linked to albinism were identified in 11 individuals (7%), including three truncating variants in PMEL, reinforcing the role of pigmentation pathways in cutaneous melanoma susceptibility. Two patients carried mutations in MBD4, suggesting it may contribute to early-onset disease. The high frequency of rare variants in high- or intermediate-risk genes highlights the importance of including such genes in genetic tests, as they may have implications for future risk in the adolescent patients and their at-risk relatives.

Indexed as

Cyclin-Dependent Kinase Inhibitor p16Germ-Line MutationMelanomaSkin NeoplasmsAdolescentChildChild, PreschoolCutaneous Malignant MelanomaFemaleGenetic Predisposition to DiseaseHumansMaleCDKN2A protein, humanCyclin-Dependent Kinase Inhibitor p16adolescentcutaneous melanomagenetic riskgermline mutationpredisposition

Identifiers

PMID41673532
PMCPMC12916466

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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.