ArticleOncogene2005
Fate of UVB-induced p53 mutations in SKH-hr1 mouse skin after discontinuation of irradiation: relationship to skin cancer development.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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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
21 citing papers in PubMed, 42 citations in OpenAlex.
- Reflectance confocal microscopy detects distinct features of field damage in chronically UV-irradiated SKH1 mouse skin.JID innovations : skin science from molecules to population health · 2026Article
- Commensal papillomavirus immunity preserves the homeostasis of highly mutated normal skin.Cancer cell · 2025Article
- T helper 2 cell-directed immunotherapy eliminates precancerous skin lesions.The Journal of clinical investigation · 2025Article
- Advancements in elucidating the pathogenesis of actinic keratosis: present state and future prospects.Frontiers in medicine · 2024Review
- Tissue memory relies on stem cell priming in distal undamaged areas.Nature cell biology · 2023Article
- Immunotherapy for the Treatment of Squamous Cell Carcinoma: Potential Benefits and Challenges.International journal of molecular sciences · 2022Review
- Review
- Protective Effects of Dietary Grape on UVB-Mediated Cutaneous Damages and Skin Tumorigenesis in SKH-1 Mice.Cancers · 2020Article
- Chemoprotective Effects of Dietary Grape Powder on UVB Radiation-Mediated Skin Carcinogenesis in SKH-1 Hairless Mice.The Journal of investigative dermatology · 2019Article
- Role of p53 in silibinin-mediated inhibition of ultraviolet B radiation-induced DNA damage, inflammation and skin carcinogenesis.Carcinogenesis · 2017Article
- MIF antagonist (CPSI-1306) protects against UVB-induced squamous cell carcinoma.Molecular cancer research : MCR · 2014Article
- Tumor-promoting role of TGFβ1 signaling in ultraviolet B-induced skin carcinogenesis is associated with cutaneous inflammation and lymph node migration of dermal dendritic cells.Carcinogenesis · 2014Article
- Slug expression in mouse skin and skin tumors is not regulated by p53.The Journal of investigative dermatology · 2014Article
- The TGFβ1 pathway is required for NFκB dependent gene expression in mouse keratinocytes.Cytokine · 2013Article
- Oxidative stress and skin cancer: an overview.Indian journal of clinical biochemistry : IJCB · 2013Review
- P53 mutation is a rare event in Merkel cell carcinoma of the head and neck.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2011Article
- Reduction of IKKalpha expression promotes chronic ultraviolet B exposure-induced skin inflammation and carcinogenesis.The American journal of pathology · 2010Article
- Establishment and characterization of an osteopontin-null cutaneous squamous cell carcinoma cell line.In vitro cellular & developmental biology. Animal · 2010Article
- The hairless mouse in skin research.Journal of dermatological science · 2009Review
- Role of p53 and CDKN2A inactivation in human squamous cell carcinomas.Journal of biomedicine & biotechnology · 2007Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Chronic exposure to ultraviolet (UV) radiation causes skin cancer in humans and mice. We have previously shown that in hairless SKH-hr1 mice, UVB-induced p53 mutations arise very early, well before tumor development. In this study, we investigated whether discontinuation of UVB exposure before the onset of skin tumors results in the disappearance of p53 mutations in the skin of hairless SKH-hr1 mice. Irradiation of mice at a dose of 2.5 kJ/m2 three times a week for 8 weeks induced p53 mutations in the epidermal keratinocytes of 100% of the mice. UVB irradiation was discontinued after 8 weeks, but p53 mutations at most hotspot codons were still present even 22 weeks later. During that period, the percent of mice carrying p53(V154A/R155C), p53(H175H/H176Y), and p53R275C mutant alleles remained at or near 100%, whereas the percentage of mice with p53R270C mutation decreased by 45%. As expected, discontinuation of UVB after 8 weeks resulted in a delay in tumor development. A 100% of tumors carried p53(V154A/R155C) mutant alleles, 76% carried p53(H175H/H176Y) mutants, and 24 and 19% carried p53R270C and p53R275C mutants, respectively. These results suggest that different UVB-induced p53 mutants may provide different survival advantages to keratinocytes in the absence of further UVB exposure and that skin cancer development can be delayed but not prevented by avoidance of further exposure to UVB radiation.
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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.