Evidence map›Paper›PMID 28467800›Full record

ReviewOncotarget2017

Redirecting tumor-associated macrophages to become tumoricidal effectors as a novel strategy for cancer therapy.

Xiang Zheng, Kati Turkowski, Javier Mora, Bernhard Brüne, Werner Seeger, Andreas Weigert, Rajkumar Savai

Open access · diamondAbstract readReview
In one paragraph

Review in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 160 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
160citing papers in PubMed, 2 pooled it
13.2field-weighted citation impact, top 1% 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

160 citing papers in PubMed, 2 syntheses or guidelines pooled it, 275 citations in OpenAlex.

  1. Prognostic Role of CD68British journal of biomedical science · 2023
    Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Review
  19. Phosphatidylserine externalization as immune checkpoint in cancer.Pflugers Archiv : European journal of physiology · 2024
    Review
  20. Review

100 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

Xiang ZhengMax Planck Institute for Heart and Lung Research, Department of Lung Development and Remodeling, Member of the German Center for Lung Research (DZL), Bad Nauheim, Germany.
Kati TurkowskiMax Planck Institute for Heart and Lung Research, Department of Lung Development and Remodeling, Member of the German Center for Lung Research (DZL), Bad Nauheim, Germany.
Javier MoraInstitute of Biochemistry I, Goethe-University Frankfurt, Frankfurt, Germany.
Bernhard BrüneInstitute of Biochemistry I, Goethe-University Frankfurt, Frankfurt, Germany.
Werner SeegerMax Planck Institute for Heart and Lung Research, Department of Lung Development and Remodeling, Member of the German Center for Lung Research (DZL), Bad Nauheim, Germany.
Andreas WeigertInstitute of Biochemistry I, Goethe-University Frankfurt, Frankfurt, Germany.
Rajkumar SavaiMax Planck Institute for Heart and Lung Research, Department of Lung Development and Remodeling, Member of the German Center for Lung Research (DZL), Bad Nauheim, Germany.
Goethe University Frankfurt · DEGerman Center for Lung Research · DEMax Planck Institute for Heart and Lung Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer research in recent decades has highlighted the potential influence of the tumor microenvironment on the progression and metastasis of most known cancer types. Within the established microenvironment, tumor-associated macrophages (TAMs) are one of the most abundant and crucial non-neoplastic cell types. The polarization of macrophages into tumor-suppressive M1 or tumor-promoting M2 types is a fundamental event in the establishment of the tumor microenvironment. Although ample evidence indicates that TAMs are primarily M2 polarized, the mechanisms responsible for the regulation and maintenance of M1 and M2 polarization imbalance remain unclear. The manipulation of this critical axis through three main approaches may provide new strategies for cancer therapy - (I) specific interference with M2-like TAM survival or inhibiting their signaling cascades, (II) repression of macrophage recruitment to tumors, and (III) repolarization of tumor-promoting M2-like TAMs to a tumoricidal M1-like phenotype. This review summarizes current strategies for cancer intervention via manipulation of macrophage polarization, with particular focus on composition of the tumor microenvironment and its influence on cancer progression and metastasis. It is clear that additional fundamental and preclinical research is required to confirm the efficacy and practicality of this novel and promising strategy for treating cancer.

Indexed as

Tumor MicroenvironmentAnimalsDisease ProgressionHumansImmune SystemImmunotherapyMacrophagesNeoplasm MetastasisNeoplasmsTreatment Outcomecancer progressionmacrophagesmetastasisrepolarizationtumor microenvironment

Identifiers

PMID28467800
PMCPMC5564660
OpenAlexW2606694952

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.