ArticleOncogene2012
Myc, Aurora Kinase A, and mutant p53(R172H) co-operate in a mouse model of metastatic skin carcinoma.
Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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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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.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Integrative bioinformatics analysis of WDHD1: a potential biomarker for pan-cancer prognosis, diagnosis, and immunotherapy.World journal of surgical oncology · 2023Article
- Amplifications of AURKA and AURKB in a Burkitt lymphoma immunodeficiency-associated type: a case report.Einstein (Sao Paulo, Brazil) · 2023Article
- Review
- Rab11-FIP1/RCP Functions as a Major Signalling Hub in the Oncogenic Roles of Mutant p53 in Cancer.Frontiers in oncology · 2021Article
- Review
- 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
- Cancer Stem Cells in Squamous Cell Carcinoma.The Journal of investigative dermatology · 2017Review
- Article
- Combined Tumor Suppressor Defects Characterize Clinically Defined Aggressive Variant Prostate Cancers.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Article
- Article
- Article
- Mantle cell lymphoma harboring Burkitt's-like translocations presents differential expression of aurora kinase genes compared with others 8q abnormalities.Medical oncology (Northwood, London, England) · 2014Article
- Two hot spot mutant p53 mouse models display differential gain of function in tumorigenesis.Cell death and differentiation · 2013Article
- Loss of PML cooperates with mutant p53 to drive more aggressive cancers in a gender-dependent manner.Cell cycle (Georgetown, Tex.) · 2013Article
- Aurora A kinase (AURKA) in normal and pathological cell division.Cellular and molecular life sciences : CMLS · 2013Review
- Aurora kinase-A deficiency during skin development impairs cell division and stratification.The Journal of investigative dermatology · 2013Article
- Chronic low dose UV exposure and p53 mutation: tilting the odds in early epidermal preneoplasia?International journal of radiation biology · 2012Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Clinical observations, as well as data obtained from the analysis of genetically engineered mouse models, firmly established the gain-of-function (GOF) properties of certain p53 mutations. However, little is known about the underlying mechanisms. We have used two independent microarray platforms to perform a comprehensive and global analysis of tumors arising in a model of metastatic skin cancer progression, which compares the consequences of a GOF p53(R172H) mutant vs p53 deficiency. DNA profiling revealed a higher level of genomic instability in GOF vs loss-of-function (LOF) p53 squamous cell carcinomas (SCCs). Moreover, GOF p53 SCCs showed preferential amplification of Myc with a corresponding increase in its expression and deregulation of Aurora Kinase A. Fluorescent in situ hybridization confirmed amplification of Myc in primary GOF p53 SCCs and its retention in metastatic tumors. We also identified by RNA profiling distinct gene expression profiles in GOF p53 tumors, which included enriched integrin and Rho signaling, independent of tumor stage. Thus, the progression of GOF p53 papillomas to carcinoma was marked by the acquisition of epithelial-to-mesenchymal transition and metastatic signatures. In contrast, LOF p53 tumors showed enrichment of genes associated with cancer proliferation and chromosomal instability. Collectively, these observations suggest that genomic instability has a prominent role in the early stages of GOF p53 tumor progression (that is, papillomas), whereas it is implicated at a later stage in LOF p53 tumors (that is, SCCs). This model will allow us to identify specific targets in mutant p53 SCCs, which may lead to the development of new therapeutic agents for the treatment of metastatic SCCs.
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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.