Evidence map›Paper›PMID 30185657›Full record

ArticleJCI insight2018

Ruxolitinib inhibits cyclosporine-induced proliferation of cutaneous squamous cell carcinoma.

Melody Abikhair Burgo, Nazanin Roudiani, Jie Chen, Alexis L Santana, Nicole Doudican, Charlotte Proby, Diane Felsen, John A Carucci

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

15 citing papers in PubMed, 35 citations in OpenAlex.

  1. Trial
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  12. Cutaneous Squamous Cell Carcinoma: From Biology to Therapy.International journal of molecular sciences · 2020
    Review
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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

8 authors at 3 institutions in 2 countries.

Melody Abikhair BurgoRonald O. Perelman Department of Dermatology, New York University School of Medicine, New York, New York, USA.
Nazanin RoudianiRonald O. Perelman Department of Dermatology, New York University School of Medicine, New York, New York, USA.
Jie ChenInstitute for Pediatric Urology, Department of Urology, Weill Cornell Medicine, New York, New York, USA.
Alexis L SantanaRonald O. Perelman Department of Dermatology, New York University School of Medicine, New York, New York, USA.
Nicole DoudicanRonald O. Perelman Department of Dermatology, New York University School of Medicine, New York, New York, USA.
Charlotte ProbyDivision of Cancer Research, Jacqui Wood Cancer Centre, University of Dundee, Dundee, Scotland, United Kingdom.
Diane FelsenInstitute for Pediatric Urology, Department of Urology, Weill Cornell Medicine, New York, New York, USA.
John A CarucciRonald O. Perelman Department of Dermatology, New York University School of Medicine, New York, New York, USA.
New York University · USCornell University · USUniversity of Dundee · GB

Funding

Cutaneous Biology and Skin Disease Training ProgramT32AR064184 · NIAMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ORLOW, SETH J. · 2014 to 2024
$2.1M
NIAMS NIH HHS T32 AR064184
6 · The paper itself

Abstract

Organ transplant recipients (OTRs) on cyclosporine A (CSA) are prone to catastrophic cutaneous squamous cell carcinoma (SCC). Allograft-sparing, cancer-targeting systemic treatments are unavailable. We have shown increased risk for catastrophic SCC in OTRs via CSA-mediated induction of IL-22. Herein, we found that CSA drives SCC proliferation and tumor growth through IL-22 and JAK/STAT pathway induction. We in turn inhibited SCC growth with an FDA-approved JAK1/2 inhibitor, ruxolitinib. In human SCC cells, the greatest proliferative response to IL-22 and CSA treatment occurred in nonmetastasizing lines. IL-22 treatment upregulated JAK1 and STAT1/3 in A431 SCC cells. JAK/STAT pathway genes were highly expressed in tumors from a cohort of CSA-exposed OTRs and in SCC with high risk for metastasis. Compared with immunocompetent SCC, genes associated with innate immunity, response to DNA damage, and p53 regulation were differentially expressed in SCC from OTRs. In nude mice engrafted with human A431 cells, IL-22 and CSA treatment increased tumor growth and upregulated IL-22 receptor, JAK1, and STAT1/3 expression. Ruxolitinib treatment significantly reduced tumor volume and reversed the accelerated tumor growth. CSA and IL-22 exacerbate aggressive behavior in SCC. Targeting the IL-22 axis via selective JAK/STAT inhibition may reduce the progression of aggressive SCC in OTRs, without compromising immunosuppression.

Indexed as

AnimalsCarcinoma, Squamous CellCell Line, TumorCell ProliferationCyclosporineDisease Models, AnimalDisease ProgressionFemaleGene Expression Regulation, NeoplasticHeterograftsHumansInterleukin-22InterleukinsJanus Kinase 1MiceMice, NudeCyclosporineInterleukin-22interleukin-22 receptorInterleukinsJak1 protein, mouseJanus Kinase 1NitrilesPyrazolesPyrimidinesReceptors, InterleukinruxolitinibStat1 protein, mouseSTAT1 Transcription FactorStat3 protein, mouseSTAT3 Transcription FactorDermatologyDrug therapyOrgan transplantationSkin cancerTransplantation

Identifiers

PMID30185657
PMCPMC6171807
OpenAlexW2889720040

What OpenQuestion holds

Textmetadata
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.