Evidence map›Paper›PMID 33888854›Full record

ArticleScientific reports2021

Transcriptomic analysis identifies differences in gene expression in actinic keratoses after treatment with imiquimod and between responders and non responders.

Megan H Trager, Emanuelle Rizk, Sharon Rose, Kuixi Zhu, Branden Lau, Benjamin T Fullerton, Jaya Pradhan, Michael Moore, Ayush C Srivastava, Giselle Singer and 5 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 42% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Review
  2. Article
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

15 authors at 3 institutions in 1 country.

Megan H Trager *Department of Dermatology, Columbia University Irving Medical Center, New York, NY, USA.
Emanuelle Rizk *Department of Medicine, Division of Hematology/Oncology, Columbia University Irving Medical Center, New York, NY, USA.
Sharon Rose *Department of Dermatology, Mount Sinai Hospital, New York, NY, USA.
Kuixi Zhu *Department of Neurology, University of Arizona Health Sciences, Tucson, AZ, USA.
Branden LauDepartment of Neurology, University of Arizona Health Sciences, Tucson, AZ, USA.
Benjamin T FullertonDepartment of Medicine, Division of Hematology/Oncology, Columbia University Irving Medical Center, New York, NY, USA.
Jaya PradhanDepartment of Pathology, Columbia University Irving Medical Center, New York, NY, USA.
Michael MooreDepartment of Surgery, Columbia University Irving Medical Center, New York, NY, USA.
Ayush C SrivastavaDepartment of Medicine, Division of Hematology/Oncology, Columbia University Irving Medical Center, New York, NY, USA.
Giselle SingerDepartment of Dermatology, Mount Sinai Hospital, New York, NY, USA.
Robyn GartrellDepartment of Pediatrics, Division of Hematology/Oncology, Columbia University Irving Medical Center, New York, NY, USA.
Rui Chang *Department of Neurology, University of Arizona Health Sciences, Tucson, AZ, USA.
Larisa J Geskin *Department of Dermatology, Columbia University Irving Medical Center, New York, NY, USA.
Yvonne M Saenger *Department of Medicine, Division of Hematology/Oncology, Columbia University Irving Medical Center, New York, NY, USA. yms4@cumc.columbia.edu.
Gary Goldenberg *Department of Dermatology, Mount Sinai Hospital, New York, NY, USA.
Columbia University Irving Medical Center · USMount Sinai Hospital · USUniversity of Arizona · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The presence of actinic keratoses (AKs) increases a patient's risk of developing squamous cell carcinoma by greater than six-fold. We evaluated the effect of topical treatment with imiquimod on the tumor microenvironment by measuring transcriptomic differences in AKs before and after treatment with imiquimod 3.75%. Biopsies were collected prospectively from 21 patients and examined histologically. RNA was extracted and transcriptomic analyses of 788 genes were performed using the nanoString assay. Imiquimod decreased number of AKs by study endpoint at week 14 (p < 0.0001). Post-imiquimod therapy, levels of CDK1, CXCL13, IL1B, GADPH, TTK, ILF3, EWSR1, BIRC5, PLAUR, ISG20, and C1QBP were significantly lower (adjusted p < 0.05). Complete responders (CR) exhibited a distinct pattern of inflammatory gene expression pre-treatment relative to incomplete responders (IR), with alterations in 15 inflammatory pathways (p < 0.05) reflecting differential expression of 103 genes (p < 0.05). Presence of adverse effects was associated with improved treatment response. Differences in gene expression were found between pre-treatment samples in CR versus IR, suggesting that higher levels of inflammation pre-treament may play a part in regression of AKs. Further characterization of the immune micro-environment in AKs may help develop biomarkers predictive of response to topical immune modulators and may guide therapy.

Indexed as

Gene ExpressionTranscriptomeAdjuvants, ImmunologicAdministration, TopicalAgedAged, 80 and overBiopsyFemaleHumansImiquimodKeratosis, ActinicMaleMiddle AgedTreatment OutcomeAdjuvants, ImmunologicImiquimod

Identifiers

PMID33888854
PMCPMC8062619
OpenAlexW3156858857

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Registered trials

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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.