ReviewToxicology and applied pharmacology2007
p53 and the pathogenesis of skin cancer.
Review in Toxicology and applied pharmacology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
67 citing papers in PubMed, 2 syntheses or guidelines pooled it, 207 citations in OpenAlex.
- Pooled it
- Pooled it
- Enhanced Lichenysin Production in Bacillus licheniformis by Physicochemical Mutagenesis Combined with High-Throughput Screening.Current microbiology · 2026Article
- Review
- Assessing phototoxic drug properties of hydrochlorothiazide using human skin biopsies.Communications biology · 2025Article
- Emerging Technologies for Timely Point-of-Care Diagnostics of Skin Cancer.Global challenges (Hoboken, NJ) · 2025Review
- Exploring the association between dietary inflammatory index (DII) and different types of skin cancer: a cross-sectional study from NHANES 1999-2018.European journal of nutrition · 2025Article
- The evolving landscape of laser-based skin cancer prevention.Lasers in medical science · 2025Review
- Illuminating the Connection: Cutaneous Vitamin DNutrients · 2025Review
- Biological and Therapeutic Responses of Human Skin to Different Wavelengths of Light: A Comprehensive Review.Journal of lasers in medical sciences · 2025Review
- Natural Compounds for Preventing Age-Related Diseases and Cancers.International journal of molecular sciences · 2024Review
- Skin Cancer Risk of Narrow-Band UV-B (TL-01) Phototherapy: A Multi-Center Registry Study with 4,815 Patients.Acta dermato-venereologica · 2024Article
- Ultraviolet Radiation Biological and Medical Implications.Current issues in molecular biology · 2024Review
- The art of war: using genetic insights to understand and harness radiation sensitivity in hematologic malignancies.Frontiers in oncology · 2024Review
- Polymeric Nanoparticles as Tunable Nanocarriers for Targeted Delivery of Drugs to Skin Tissues for Treatment of Topical Skin Diseases.Pharmaceutics · 2023Review
- An update on clinical trials for chemoprevention of human skin cancer.Journal of cancer metastasis and treatment · 2023Article
- TP53 and its Regulatory Genes as Prognosis of Cutaneous Melanoma.Cancer informatics · 2023Article
- Novel Approaches in Non-Melanoma Skin Cancers-A Focus on Hedgehog Pathway in Basal Cell Carcinoma (BCC).Cells · 2022Review
- AGO-RBP crosstalk on target mRNAs: Implications in miRNA-guided gene silencing and cancer.Translational oncology · 2022Review
- Molecular Mechanisms of Cutaneous Squamous Cell Carcinoma.International journal of molecular sciences · 2022Review
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The p53 tumor suppressor gene and gene product are among the most diverse and complex molecules involved in cellular functions. Genetic alterations within the p53 gene have been shown to have a direct correlation with cancer development and have been shown to occur in nearly 50% of all cancers. p53 mutations are particularly common in skin cancers and UV irradiation has been shown to be a primary cause of specific 'signature' mutations that can result in oncogenic transformation. There are certain 'hot-spots' in the p53 gene where mutations are commonly found that result in a mutated dipyrimidine site. This review discusses the role of p53 from normal function and its dysfunction in pre-cancerous lesions and non-melanoma skin cancers. Additionally, special situations are explored, such as Li-Fraumeni syndrome in which there is an inherited p53 mutation, and the consequences of immune suppression on p53 mutations and the resulting increase in non-melanoma skin cancer in these patients.
Indexed as
Identifiers
What OpenQuestion holds
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.