ArticleThe Journal of clinical investigation2007
An inducible mouse model for skin cancer reveals distinct roles for gain- and loss-of-function p53 mutations.
Article in The Journal of clinical investigation, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 143 citations in OpenAlex.
- Review
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- RAS oncogene signal strength regulates matrisomal gene expression and tumorigenicity of mouse keratinocytes.Carcinogenesis · 2022Article
- Dichotomous role of miR193b-3p in diabetic foot ulcers maintains inhibition of healing and suppression of tumor formation.Science translational medicine · 2022Article
- Zebrafish imaging reveals TP53 mutation switching oncogene-induced senescence from suppressor to driver in primary tumorigenesis.Nature communications · 2022Article
- Review
- The role of Hippo-YAP signaling in squamous cell carcinomas.Cancer science · 2021Review
- Genetic mutation profile of Chinese HER2-positive breast cancers and genetic predictors of responses to Neoadjuvant anti-HER2 therapy.Breast cancer research and treatment · 2020Article
- OncogenicLife science alliance · 2020Article
- YAP1 is a potent driver of the onset and progression of oral squamous cell carcinoma.Science advances · 2020Article
- Gain-of-Function Mutations in p53 in Cancer Invasiveness and Metastasis.International journal of molecular sciences · 2020Review
- Article
- Gain-of-Function Mutant p53: All the Roads Lead to Tumorigenesis.International journal of molecular sciences · 2019Review
- Trp53 null and R270H mutant alleles have comparable effects in regulating invasion, metastasis, and gene expression in mouse colon tumorigenesis.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- Targeted Therapy Against the Cell of Origin in Cutaneous Squamous Cell Carcinoma.International journal of molecular sciences · 2019Review
- Activation of S6 signaling is associated with cell survival and multinucleation in hyperplastic skin after epidermal loss of AURORA-A Kinase.Cell death and differentiation · 2019Article
- Considerations for skin carcinogenesis experiments using inducible transgenic mouse models.BMC research notes · 2018Article
- HPV-Induced Field Cancerisation: Transformation of Adult Tissue Stem Cell Into Cancer Stem Cell.Frontiers in microbiology · 2018Article
- Li-Fraumeni Syndrome Disease Model: A Platform to Develop Precision Cancer Therapy Targeting Oncogenic p53.Trends in pharmacological sciences · 2017Review
10 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Mutations in ras and p53 are the most prevalent mutations found in human nonmelanoma skin cancers. Although some p53 mutations cause a loss of function, most result in expression of altered forms of p53, which may exhibit gain-of-function properties. Therefore, understanding the consequences of acquiring p53 gain-of-function versus loss-of-function mutations is critical for the generation of effective therapies for tumors harboring p53 mutations. Here we describe an inducible mouse model in which skin tumor formation is initiated by activation of an endogenous K-ras(G12D) allele. Using this model we compared the consequences of activating the p53 gain-of-function mutation p53(R172H) and of deleting the p53 gene. Activation of the p53(R172H) allele resulted in increased skin tumor formation, accelerated tumor progression, and induction of metastasis compared with deletion of p53. Consistent with these observations, the p53(R172H) tumors exhibited aneuploidy associated with centrosome amplification, which may underlie the mechanism by which p53(R172H) exerts its oncogenic properties. These results clearly demonstrate that p53 gain-of-function mutations confer poorer prognosis than loss of p53 during skin carcinogenesis and have important implications for the future design of therapies for tumors that exhibit p53 gain-of-function mutations.
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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.