Evidence map›Paper›PMID 25594066›Full record

ArticleOncoscience2014

An old friend with new skills: Imiquimod as novel inhibitor of Hedgehog signaling in basal cell carcinoma.

Wolfgang Gruber, Anna-Maria Frischauf, Fritz Aberger

Open access · bronzeAbstract read
In one paragraph

Article in Oncoscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

11 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Triple Hedgehog Pathway Inhibition for Basal Cell Carcinoma.The Journal of clinical and aesthetic dermatology · 2017
    Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. 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

3 authors at 1 institution in 1 country.

Wolfgang GruberDepartment of Molecular Biology, Division of Molecular Tumor Biology, University of Salzburg, Salzburg, Austria.
Anna-Maria FrischaufDepartment of Molecular Biology, Division of Molecular Tumor Biology, University of Salzburg, Salzburg, Austria.
Fritz AbergerDepartment of Molecular Biology, Division of Molecular Tumor Biology, University of Salzburg, Salzburg, Austria.
University of Salzburg · AT

Funding

Austrian Science Fund FWF P 20652Austrian Science Fund FWF P 25629
6 · The paper itself

Abstract

Deregulated Hedgehog (HH)/GLI signaling plays an etiologic role in the initiation, progression and maintenance of many cancers. Small molecule targeting of HH signaling by inhibiting the essential pathway effector Smoothened (SMO) has proven exceptionally efficient for the treatment of advanced and metastatic basal cell carcinoma. That said, severe side effects, limited response rates, SMO-independent GLI signaling and rapid development of drug resistance limit the therapeutic success of SMO antagonists, urgently calling for the identification of alternative and additional strategies repressing oncogenic HH signaling. In this perspective article we highlight recent findings showing that the Toll-like receptor-7/8 (TLR7/8) agonist imiquimod (IMQ), an immune modulator approved for the treatment of basal cell carcinoma, can also act as a potent cell autonomous inhibitor of oncogenic HH signaling. Surprisingly, IMQ reduces HH signal strength independent of TLR signaling, via adenosine receptor (ADORA)/Adenylate cyclase (AC)/Protein kinase A (PKA) activation. We here highlight the molecular mechanisms of IMQ-mediated repression of HH/GLI and discuss the possible benefits as well as challenges of using ADORA agonists for the treatment of HH-associated cancer.

Indexed as

Adenosine receptorsADORAbasal cell carcinomaGLI proteinsHedgehog signalingImiquimodPKAProtein Kinase A

Identifiers

PMID25594066
PMCPMC4278338
OpenAlexW2182198647

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.