ArticleCancer discovery2015
CDKN2B Loss Promotes Progression from Benign Melanocytic Nevus to Melanoma.
Article in Cancer discovery, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.
- Genomics of Primary and Metastatic Cutaneous Melanoma: A Systematic Review and Meta-Analysis.American journal of clinical dermatology · 2026Pooled it
- Large-scale pleiotropic analysis across cancers reveals shared genetic mechanisms and identifies novel functional genes.Briefings in bioinformatics · 2026Article
- Article
- The Wnt signaling networks in higher-grade meningiomas: from molecular pathogenesis to therapeutic innovation.Cancer cell international · 2026Review
- Disruption of CTCF binding by germline non-coding variants inmedRxiv : the preprint server for health sciences · 2026Article
- Rapid activation of ARF6 after RAF inhibition augments BRAFOncogene · 2026Article
- A high-penetrance intergenic variant at 9p21 confers melanoma susceptibility.Research square · 2026Article
- Stress vesicles link epidermal mechanotransduction to stem cell differentiation.Nature communications · 2026Article
- Rapid activation of ARF6 after RAF inhibition augments BRAFV600E and promotes therapy resistance.Research square · 2025Article
- Crosstalk in Skin: Loss of Desmoglein 1 in Keratinocytes Inhibits BRAFThe Journal of investigative dermatology · 2025Article
- A CDKN2B-Associated Immune Prognostic Model for Predicting Immune Cell Infiltration and Prognosis in Esophageal Carcinoma.Clinical and experimental gastroenterology · 2025Article
- Exploring the Common Mutational Landscape in Cutaneous Melanoma and Pancreatic Cancer.Pigment cell & melanoma research · 2025Review
- Article
- High frequency of melanoma inTheranostics · 2024Article
- Landscape of enhancer disruption and functional screen in melanoma cells.Genome biology · 2023Article
- The journey from melanocytes to melanoma.Nature reviews. Cancer · 2023Review
- Localized immune surveillance of primary melanoma in the skin deciphered through executable modeling.Science advances · 2023Article
- TP53 and its Regulatory Genes as Prognosis of Cutaneous Melanoma.Cancer informatics · 2023Article
- Targeting anti-apoptotic pathways eliminates senescent melanocytes and leads to nevi regression.Nature communications · 2022Article
- Screening of potential novel candidate genes in schwannomatosis patients.Human mutation · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
unlabelledDeletion of the entire CDKN2B-CDKN2A gene cluster is among the most common genetic events in cancer. The tumor-promoting effects are generally attributed to loss of CDKN2A-encoded p16 and p14ARF tumor suppressors. The degree to which the associated CDKN2B-encoded p15 loss contributes to human tumorigenesis is unclear. Here, we show that CDKN2B is highly upregulated in benign melanocytic nevi, contributes to maintaining nevus melanocytes in a growth-arrested premalignant state, and is commonly lost in melanoma. Using primary melanocytes isolated directly from freshly excised human nevi naturally expressing the common BRAF(V600E)-activating mutation, nevi progressing to melanoma, and normal melanocytes engineered to inducibly express BRAF(V600E), we show that BRAF activation results in reversible, TGFβ-dependent, p15 induction that halts proliferation. Furthermore, we engineer human skin grafts containing nevus-derived melanocytes to establish a new, architecturally faithful, in vivo melanoma model, and demonstrate that p15 loss promotes the transition from benign nevus to melanoma. SIGNIFICANCE: Although BRAF(V600E) mutations cause melanocytes to initially proliferate into benign moles, mechanisms responsible for their eventual growth arrest are unknown. Using melanocytes from human moles, we show that BRAF activation leads to a CDKN2B induction that is critical for restraining BRAF oncogenic effects, and when lost, contributes to melanoma.
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Registered trials
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.