Evidence map›Paper›PMID 36394590›Full record

ReviewDermatologie (Heidelberg, Germany)2022

[Melanoma-associated macrophages-from molecular signals to therapeutic application].

Eftychia Chatziioannou, Serra Atilla Aydin, Stephan Forchhammer, Tobias Sinnberg, Thomas Eigentler

Abstract readEnglish AbstractReview
PubMed Publisher
In one paragraph

Review in Dermatologie (Heidelberg, Germany), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.5field-weighted citation impact, top 38% 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

7 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Cell Immunotherapy against Melanoma: Clinical Trials Review.International journal of molecular sciences · 2023
    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

5 authors at 3 institutions in 1 country.

Eftychia ChatziioannouUniversitätshautklinik, Universitätsklinikum Tübingen, Liebermeisterstr. 25, 72076, Tübingen, Deutschland.
Serra Atilla AydinKlinik für Dermatologie, Venerologie und Allergologie, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt Universität zu Berlin, Luisenstr. 2, 10117, Berlin, Deutschland.
Stephan ForchhammerUniversitätshautklinik, Universitätsklinikum Tübingen, Liebermeisterstr. 25, 72076, Tübingen, Deutschland.
Tobias SinnbergUniversitätshautklinik, Universitätsklinikum Tübingen, Liebermeisterstr. 25, 72076, Tübingen, Deutschland.
Thomas EigentlerKlinik für Dermatologie, Venerologie und Allergologie, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt Universität zu Berlin, Luisenstr. 2, 10117, Berlin, Deutschland. thomas.eigentler@charite.de.
Charité - Universitätsmedizin Berlin · DEUniversitätsklinikum Tübingen · DEFreie Universität Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMacrophages are an important component of the innate immune system. They are abbreviated as Mφ, MΦ, or MP. The name is derived from Greek: large eaters, μακρóς (makrós) = large, φαγεῖν (phagein) = to eat, because they engulf and digest pathogens. Tumor-associated macrophages (TAMs) are associated with drug resistance in cancers, including melanoma, and targeting them may improve cancer treatment.

objectivesThe purpose of this article is to examine the role of TAMs in cancer, particularly in melanoma. The relationship between TAM and treatment resistance and their potential application in the treatment of melanoma are discussed. MATERIALS AND

methodsA literature search in PubMed and Google Scholar databases for TAM and melanoma was performed. Clinical trials were searched via clinicaltrials.gov and graphical representations were created using BioRender.

resultsIn melanoma, macrophages are among the most abundant immune cells in the tumor microenvironment (TME). TAMs are associated with poor prognosis and resistance. They are involved in tumorigenesis and metastasis development. M2 is the predominant type of TAM and the M2 markers CD163 and CD204 are unfavorable prognostic biomarkers. Therapeutic approaches aim to decrease their recruitment, modulate their function, or reprogram them. Treatment using chimeric antigen receptor (CAR)-M cells and nanoparticles are currently being investigated. Drugs being tested for melanoma include signal transducer and activator of transcription 3 (STAT3) inhibitors, macrophage colony-stimulating factor (M-CSF) antagonists, interferons (IFN), talimogene laherparepvec (TVEC), histone deacetylase (HDAC) inhibitors, indoleamine 2,3-dioxygenase (IDO) inhibitors, colony-stimulating factor 1 receptor (CSF-1R) antagonists, CD40 agonists, arginase 1 (ARG-1) inhibitors, and phosphoinositide 3‑kinase γ (PI3K-γ) inhibitors.

conclusionsTAMs participate in developing resistance to current melanoma therapies. Treatment directed against them may help reduce the development of resistance and improve survival.

Indexed as

MelanomaOncolytic VirotherapyHumansMacrophagesPhosphatidylinositol 3-KinasesTumor MicroenvironmentPhosphatidylinositol 3-KinasesImmunotherapy resistanceInnate immunityMagrophage-targeting strategiesTumor-associated macrophagesTumor microenvironment

Identifiers

PMID36394590
OpenAlexW4309242692

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.