ArticleThe Journal of investigative dermatology2015
Multifaceted contributions of epidermal langerhans cells to cutaneous carcinogenesis.
Article in The Journal of investigative dermatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 7 citations in OpenAlex.
- From neglect to necessity: the role of innate immunity in cutaneous squamous cell carcinoma therapy.Frontiers in immunology · 2025Review
- Pak1 maintains epidermal stem cells by regulating Langerhans cells and is required for skin carcinogenesis.Oncogene · 2020Article
- Functional Specialization of Skin Dendritic Cell Subsets in Regulating T Cell Responses.Frontiers in immunology · 2015Review
Corrections and comments
- Comment on
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent findings have established that epidermal Langerhans cells (LCs) promote polyaromatic hydrocarbon (PAH)-induced carcinogenesis independent of their immunological properties by generating mutagenic PAH metabolites. In this issue, Girardi and colleagues (2014) extend their previous work and demonstrate that this mutagenic metabolism of LCs is indeed mediated by preferential expression of the cytochrome P450 enzyme CYP1B1, but that LCs cells exert their pro-carcinogenic effects also independently of CYP1B1.
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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.