ArticleOncogene1999
P16 UV mutations in human skin epithelial tumors.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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
19 citing papers in PubMed, 109 citations in OpenAlex.
- Review
- Molecular and cellular dynamics of squamous cell carcinomas across tissues.Genes & development · 2025Review
- Immunotherapy for the Treatment of Squamous Cell Carcinoma: Potential Benefits and Challenges.International journal of molecular sciences · 2022Review
- Molecular Mechanisms of Cutaneous Squamous Cell Carcinoma.International journal of molecular sciences · 2022Review
- HDAC1/2 Control Proliferation and Survival in Adult Epidermis and Pre‒Basal Cell Carcinoma through p16 and p53.The Journal of investigative dermatology · 2022Article
- Xeroderma Pigmentosum C: A Valuable Tool to Decipher the Signaling Pathways in Skin Cancers.Oxidative medicine and cellular longevity · 2021Review
- MicroRNA Dysregulation in Cutaneous Squamous Cell Carcinoma.International journal of molecular sciences · 2019Review
- Biomarkers of Cellular Senescence and Skin Aging.Frontiers in genetics · 2018Review
- Loss of INK4a/Arf gene enhances ultraviolet radiation-induced cutaneous tumor development.Experimental dermatology · 2017Article
- Reduced P53 Staining in Actinic Keratosis is Associated with Squamous Cell Carcinoma: A Preliminary Study.Indian journal of dermatology · 2013Article
- Modification of second cancer risk after malignant melanoma by parental history of cancer.British journal of cancer · 2008Article
- Allelic imbalances and microdeletions affecting the PTPRD gene in cutaneous squamous cell carcinomas detected using single nucleotide polymorphism microarray analysis.Genes, chromosomes & cancer · 2007Article
- Role of p53 and CDKN2A inactivation in human squamous cell carcinomas.Journal of biomedicine & biotechnology · 2007Article
- Mechanism of UV-related carcinogenesis and its contribution to nevi/melanoma.Expert review of dermatology · 2007Article
- NF-kappaB activation in melanoma.Pigment cell research · 2006Review
- Article
- P16(INK4A) is implicated in both the immediate and adaptative response of human keratinocytes to UVB irradiation.Oncogene · 2002Article
- Article
- Analysis of p16 expression and allelic imbalance / loss of heterozygosity of 9p21 in cutaneous squamous cell carcinomas.Journal of cellular and molecular medicineArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The p16 gene expresses two alternative transcripts (p16alpha and p16beta) involved in tumor suppression via the retinoblastoma (Rb) or p53 pathways. Disruption of these pathways can occur through inactivation of p16 or p53, or activating mutations of cyclin dependant kinase 4 gene (Cdk4). We searched for p16, Cdk4 and p53 gene mutations in 20 squamous cell carcinomas (SSCs), 1 actinic keratosis (AK), and 28 basal cell carcinomas (BCCs), using PCR-SSCP. A deletion and methylation analysis of p16 was also performed. Six different mutations (12%) were detected in exon 2 of p16 (common to p16alpha and p16beta), in five out of 21 squamous lesions (24%) (one AK and four SCCs) and one out of 28 BCCs (3.5%). These included four (66%) ultraviolet (UV)-type mutations (two tandems CC : GG to TT : AA transitions and two C : G to T : A transitions at dipyrimidic site) and two transversions. P53 mutations were present in 18 samples (37%), mostly of UV type. Of these, only two (one BCC and one AK) harboured simultaneously mutations of p16, but with no consequence on p16beta transcript. Our data demonstrate for the first time the presence of p16 UV induced mutations in non melanoma skin cancer, particularly in the most aggressive SCC type, and support that p16 and p53 are involved in two independent pathways in skin carcinogenesis.
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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.