Evidence map›Paper›PMID 26053049›Full record

ArticleThe Journal of investigative dermatology2015

Langerhans Cells Facilitate UVB-Induced Epidermal Carcinogenesis.

Julia M Lewis, Christina D Bürgler, Marianna Freudzon, Kseniya Golubets, Juliet F Gibson, Renata B Filler, Michael Girardi

Open access · bronzeAbstract read
In one paragraph

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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.2field-weighted citation impact, top 22% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Chronic UV radiation-induced RORγt+ IL-22-producing lymphoid cells are associated with mutant KC clonal expansion.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  9. Monocytes promote UV-induced epidermal carcinogenesis.European journal of immunology · 2021
    Article
  10. Review
  11. Article
  12. Article
  13. The Role of the Immune System in Cutaneous Squamous Cell Carcinoma.International journal of molecular sciences · 2019
    Review
  14. Review
  15. Article
  16. Emerging Skin T-Cell Functions in Response to Environmental Insults.The Journal of investigative dermatology · 2017
    Review
  17. Review
  18. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Julia M LewisDepartment of Dermatology, Yale School of Medicine, New Haven, Connecticut, USA.
Christina D BürglerDepartment of Dermatology, Yale School of Medicine, New Haven, Connecticut, USA.
Marianna FreudzonDepartment of Dermatology, Yale School of Medicine, New Haven, Connecticut, USA.
Kseniya GolubetsDepartment of Dermatology, Yale School of Medicine, New Haven, Connecticut, USA.
Juliet F GibsonDepartment of Dermatology, Yale School of Medicine, New Haven, Connecticut, USA.
Renata B FillerDepartment of Dermatology, Yale School of Medicine, New Haven, Connecticut, USA.
Michael GirardiDepartment of Dermatology, Yale School of Medicine, New Haven, Connecticut, USA. Electronic address: girardi@yale.edu.
Yale University · US

Funding

T Cell Regulation of Cutaneous MalignancyR01CA102703 · NCI · YALE UNIVERSITY · PI GIRARDI, MICHAEL · 2003 to 2020
$5.5M
NCI NIH HHS R01 CA102703NCI NIH HHS R01CA102703
6 · The paper itself

Abstract

UVB light is considered the major environmental inducer of human keratinocyte (KC) DNA mutations, including within the tumor-suppressor gene p53, and chronic exposure is associated with cutaneous squamous cell carcinoma formation. Langerhans cells (LCs) comprise a dendritic network within the suprabasilar epidermis, yet the role of LCs in UVB-induced carcinogenesis is largely unknown. Herein we show that LC-intact epidermis develops UVB-induced tumors more readily than LC-deficient epidermis. Although levels of epidermal cyclopyrimidine dimers following acute UVB exposure are equivalent in the presence or absence of LCs, chronic UVB-induced p53 mutant clonal islands expand more readily in association with LCs, which remain largely intact and are preferentially found in proximity to the expanding mutant KC populations. The observed LC facilitation of mutant p53 clonal expansion is completely αβ and γδ T-cell independent and is associated with increased intraepidermal expression of IL-22 and the presence of group 3 innate lymphoid cells. These data demonstrate that LCs have a key role in UVB-induced cutaneous carcinogenesis and suggest that LCs locally stimulate KC proliferation and innate immune cells that provoke tumor outgrowth.

Indexed as

AnimalsBiopsy, NeedleCarcinogenesisCell ProliferationCells, CulturedDisease Models, AnimalEpidermisFemaleFlow CytometryGene Expression RegulationHumansImmunohistochemistryInterleukin-22InterleukinsLangerhans CellsMiceInterleukin-22Interleukins

Identifiers

PMID26053049
PMCPMC4640962
OpenAlexW1595740855

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.