ArticleBritish journal of cancer2006
Cellular senescence in naevi and immortalisation in melanoma: a role for p16?
Article in British journal of cancer, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 171 papers, 1 of them a synthesis that pooled it.
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Who cites it
171 citing papers in PubMed, 1 synthesis or guideline pooled it, 387 citations in OpenAlex.
- Reconstructing the molecular life history of gliomas.Acta neuropathologica · 2018Pooled it
- Height and bone mineral density are associated with naevus count supporting the importance of growth in melanoma susceptibility.PloS one · 2015Trial
- Systematic interrogation of drug sensitivities in melanoma reveals potent synergistic and antagonistic drug combinations with translational potential.Communications medicine · 2026Article
- A Short Report on Melanocyte/Melanoma Culture, Senescence, and Reproducibility.Pigment cell & melanoma research · 2026Article
- Single-cell transcriptomic profiling of halo nevi and normal nevi reveals CD8Frontiers in immunology · 2026Article
- Balancing senescence and apoptosis: therapeutic insights into aging and cancer.Molecular and cellular biochemistry · 2025Review
- UVA-induced DNA damage and mutations in human melanocytes: relevance for melanoma mutations.Nucleic acids research · 2025Article
- Telomere length and skin cancer risk: A systematic review and meta-analysis of melanoma, basal cell carcinoma and squamous cell carcinoma.Oncology letters · 2025Article
- Uncovering minimal pathways in melanoma initiation.Nature communications · 2025Article
- NHE7 drives endometrial cancer progression by delaying senescence through cAMP/CREB/GRIN2B axis-mediated Ca²⁺ influx.Communications biology · 2025Article
- Oncogene-Induced Senescence Transcriptomes Signify Premalignant Colorectal Adenomas.Current issues in molecular biology · 2025Article
- Resolution of oncogene-induced senescence markers in HPV-infected cervical cancer tissue.BMC cancer · 2025Article
- Atrial myocyte senescence as a driver of atrial fibrillation: mechanisms and therapeutic implications.Frontiers in cell and developmental biology · 2025Review
- Alpha-synuclein knockout impairs melanoma development and alters DNA damage repair in the TG3 mouse model in a sex-dependent manner.Frontiers in oncology · 2025Article
- The paradox of senescent-marker positive cancer cells: challenges and opportunities.npj aging · 2024Review
- Multiparametric identification of putative senescent cells in skeletal muscle via mass cytometry.Cytometry. Part A : the journal of the International Society for Analytical Cytology · 2024Article
- Assessment of RAS-RAF-MAPK Pathway Mutation Status in Healthy Skin, Benign Nevi, and Cutaneous Melanomas: Pilot Study Using Droplet Digital PCR.International journal of molecular sciences · 2024Article
- Article
- Cytoplasmic Expression of p16 Is Associated with Carcinoma Breast: It Is Not an Artifact.Iranian journal of pathology · 2024Article
- Preferential killing of melanoma cells by a p16-related peptide.Biology open · 2023Article
111 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
Cellular senescence, the irreversible proliferative arrest seen in somatic cells after a limited number of divisions, is considered a crucial barrier to cancer, but direct evidence for this in vivo was lacking until recently. The best-known form of human cell senescence is attributed to telomere shortening and a DNA-damage response through p53 and p21. There is also a more rapid form of senescence, dependent on the p16-retinoblastoma pathway. p16 (CDKN2A) is a known melanoma susceptibility gene. Here, we use retrovirally mediated gene transfer to confirm that the normal form of senescence in cultured human melanocytes involves p16, since disruption of the p16/retinoblastoma pathway is required as well as telomerase activation for immortalisation. Expression (immunostaining) patterns of senescence mediators and markers in melanocytic lesions provide strong evidence that cell senescence occurs in benign melanocytic naevi (moles) in vivo and does not involve p53 or p21 upregulation, although p16 is widely expressed. In comparison, dysplastic naevi and early (radial growth-phase, RGP) melanomas show less p16 and some p53 and p21 immunostaining. All RGP melanomas expressed p21, suggesting areas of p53-mediated senescence, while most areas of advanced (vertical growth-phase) melanomas lacked both p16 and p21, implying escape from both forms of senescence (immortalisation). Moreover, nuclear p16 but not p21 expression can be induced in human melanocytes by oncogenic BRAF, as found in around 80% of naevi. We conclude that cell senescence can form a barrier to melanoma development. This also provides a potential explanation of why p16 is a melanoma suppressor gene.
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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.