ArticleOncogene2010
Somatic p16(INK4a) loss accelerates melanomagenesis.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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.
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Who cites it
40 citing papers in PubMed, 71 citations in OpenAlex.
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- BRAF-Mutated Melanoma Cell Lines Develop Distinct Molecular Signatures After Prolonged Exposure to AZ628 or Dabrafenib: Potential Benefits of the Antiretroviral Treatments Cabotegravir or Doravirine on BRAF-Inhibitor-Resistant Cells.International journal of molecular sciences · 2024Article
- Senescent cardiomyocytes contribute to cardiac dysfunction following myocardial infarction.npj aging · 2023Article
- Cell-intrinsic melanin fails to protect melanocytes from ultraviolet-mutagenesis in the absence of epidermal melanin.Pigment cell & melanoma research · 2023Article
- Endothelial senescence mediates hypoxia-induced vascular remodeling by modulating PDGFB expression.Frontiers in medicine · 2022Article
- Nanotechnology Addressing Cutaneous Melanoma: The Italian Landscape.Pharmaceutics · 2021Review
- UVB mutagenesis differs inLife science alliance · 2021Article
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- Cross-species identification of PIP5K1-, splicing- and ubiquitin-related pathways as potential targets for RB1-deficient cells.PLoS genetics · 2021Article
- p16Matrix biology : journal of the International Society for Matrix Biology · 2019Article
- Molecular background of skin melanoma development and progression: therapeutic implications.Postepy dermatologii i alergologii · 2019Review
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- Ezh2 programs TNature communications · 2018Article
- Genetic Ablation of p16American journal of respiratory cell and molecular biology · 2018Article
- Expression of p16Aging cell · 2018Article
- Spatiotemporal Labeling of Melanocytes in Mice.International journal of molecular sciences · 2018Review
- Targeting the cyclin dependent kinase and retinoblastoma axis overcomes standard of care resistance in BRAFOncotarget · 2018Article
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Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
Loss of p16(INK4a)-RB and ARF-p53 tumor suppressor pathways, as well as activation of RAS-RAF signaling, is seen in a majority of human melanomas. Although heterozygous germline mutations of p16(INK4a) are associated with familial melanoma, most melanomas result from somatic genetic events: often p16(INK4a) loss and N-RAS or B-RAF mutational activation, with a minority possessing alternative genetic alterations such as activating mutations in K-RAS and/or p53 inactivation. To generate a murine model of melanoma featuring some of these somatic genetic events, we engineered a novel conditional p16(INK4a)-null allele and combined this allele with a melanocyte-specific, inducible CRE recombinase strain, a conditional p53-null allele and a loxP-stop-loxP activatable oncogenic K-Ras allele. We found potent synergy between melanocyte-specific activation of K-Ras and loss of p16(INK4a) and/or p53 in melanomagenesis. Mice harboring melanocyte-specific activated K-Ras and loss of p16(INK4a) and/or p53 developed invasive, unpigmented and nonmetastatic melanomas with short latency and high penetrance. In addition, the capacity of these somatic genetic events to rapidly induce melanomas in adult mice suggests that melanocytes remain susceptible to transformation throughout adulthood.
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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.