ArticlePigment cell & melanoma research2013
Senescence evasion in melanoma progression: uncoupling of DNA-damage signaling from p53 activation and p21 expression.
Article in Pigment cell & melanoma research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Cellular Senescence and Immunosenescence in Melanoma: Insights From the Tumor Microenvironment.Cancer medicine · 2025Pooled it
- Downregulation of Cyclin Kinase Inhibitors p16INK4a and p27 in Conjunctival Melanomas.Investigative ophthalmology & visual science · 2026Article
- The AKT-p21 phosphorylation signaling axis confers poor prognosis and dacarbazine resistance in melanoma.Scientific reports · 2025Article
- SIRT1-Mediated Redox and Senescence Regulation in Cancer: Mechanisms and Therapeutic Implications.Antioxidants (Basel, Switzerland) · 2025Review
- Preferential killing of melanoma cells by a p16-related peptide.Biology open · 2023Article
- Cellular senescence in skin-related research: Targeted signaling pathways and naturally occurring therapeutic agents.Aging cell · 2023Review
- The Cross Talk between Cellular Senescence and Melanoma: From Molecular Pathogenesis to Target Therapies.Cancers · 2023Review
- Current Understanding of the Role of Senescent Melanocytes in Skin Ageing.Biomedicines · 2022Review
- Review
- ETS1, nucleolar and non-nucleolar TERT expression in nevus to melanoma progression.Oncotarget · 2017Article
- Melanoma cells break down LPA to establish local gradients that drive chemotactic dispersal.PLoS biology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The best-established function of the melanoma-suppressor p16 is mediation of cell senescence, a permanent arrest following cell proliferation or certain stresses. The importance of p16 in melanoma suggests indolence of the other major senescence pathway through p53. Little or no p53 is expressed in senescent normal human melanocytes, but p16-deficient melanocytes can undergo p53-mediated senescence. As p16 expression occurs in nevi but falls with progression toward melanoma, we here investigated whether p53-dependent senescence occurs at some stage and, if not, what defects were detectable in this pathway, using immunohistochemistry. Phosphorylated checkpoint kinase 2 (CHEK2) can mediate DNA-damage signaling, and under some conditions senescence, by phosphorylating and activating p53. Remarkably, we detected no prevalent p53-mediated senescence in any of six classes of lesions. Two separate defects in p53 signaling appeared common: in nevi, lack of p53 phosphorylation by activated CHEK2, and in melanomas, defective p21 upregulation by p53 even when phosphorylated.
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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.