ArticlePloS one2013
A role for NF-κB activity in skin hyperplasia and the development of keratoacanthomata in mice.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 30 citations in OpenAlex.
- Multiple Keratoacanthoma-like Syndromes: Case Report and Literature Review.Medicina (Kaunas, Lithuania) · 2024Review
- Review
- Transcriptomic Study on Human Skin Samples: Identification of Two Subclasses of Actinic Keratoses.International journal of molecular sciences · 2023Article
- Inhibition of CtBP-Regulated Proinflammatory Gene Transcription Attenuates Psoriatic Skin Inflammation.The Journal of investigative dermatology · 2022Article
- Cosmetic Syndrome Correction with Calcium Hydroxylapatite-Based Filler in Patients with Connective Tissue Dysplasia.Dermatology research and practice · 2021Article
- Effects of Skin Lightening Cream Agents - Hydroquinone and Kojic Acid, on the Skin of Adult Female Experimental Rats.Clinical, cosmetic and investigational dermatology · 2020Article
- The Direct and Indirect Roles of NF-κB in Cancer: Lessons from Oncogenic Fusion Proteins and Knock-in Mice.Biomedicines · 2018Review
- PKK deletion in basal keratinocytes promotes tumorigenesis after chemical carcinogenesis.Carcinogenesis · 2018Article
- Increased Susceptibility to Skin Carcinogenesis Associated with a Spontaneous Mouse Mutation in the Palmitoyl Transferase Zdhhc13 Gene.The Journal of investigative dermatology · 2015Article
- Keratoacanthoma of the Lip: Activation of the mTOR Pathway, Tumor Suppressor Proteins, and Tumor Senescence.Medicine · 2015Observational
- Novel CARD11 Mutations in Human Cutaneous Squamous Cell Carcinoma Lead to Aberrant NF-κB Regulation.The American journal of pathology · 2015Article
- Type II transglutaminase stimulates epidermal cancer stem cell epithelial-mesenchymal transition.Oncotarget · 2015Article
- PKK suppresses tumor growth and is decreased in squamous cell carcinoma of the skin.The Journal of investigative dermatology · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundPrevious studies have implicated NF-κB signaling in both cutaneous development and oncogenesis. However, these studies have been limited in part by the lethality that results from extreme over- or under-expression of NF-κB in available mouse models. Even cre-driven tissue specific expression of transgenes, or targeted deletion of NF-κB can cause cell death. Therefore, the present study was undertaken to evaluate a novel mouse model of enhanced NF-κB activity in the skin.
methodsA knock-in homologous recombination technique was utilized to develop a mouse model (referred to as PD mice) with increased NF-κB activity.
resultsThe data show that increased NF-κB activity leads to hyperproliferation and dysplasia of the mouse epidermis. Chemical carcinogenesis in the context of enhanced NF-κB activity promotes the development of keratoacanthomata.
conclusionOur findings support an important role for NF-κB in keratinocyte dysplasia. We have found that enhanced NF-κB activity renders keratinocytes susceptible to hyperproliferation and keratoacanthoma (KA) development but is not sufficient for transformation and SCC development. We therefore propose that NF-κB activation in the absence of additional oncogenic events can promote TNF-dependent, actinic keratosis-like dysplasia and TNF-independent, KAs upon chemical carcinogensis. These studies suggest that resolution of KA cannot occur when NF-κB activation is constitutively enforced.
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.