Evidence map›Paper›PMID 32162012›Full record

ReviewInflammation research : official journal of the European Histamine Research Society ... [et al.]2020

Tumor-derived exosomes in the regulation of macrophage polarization.

Mirza S Baig, Anjali Roy, Sajjan Rajpoot, Dongfang Liu, Rajkumar Savai, Sreeparna Banerjee, Manabu Kawada, Syed M Faisal, Rohit Saluja, Uzma Saqib and 2 more

Open access · greenAbstract readReview
PubMed Publisher
In one paragraph

Review in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 163 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
163citing papers in PubMed, 2 pooled it
12.6field-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

163 citing papers in PubMed, 2 syntheses or guidelines pooled it, 264 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. Review

103 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

12 authors at 8 institutions in 5 countries.

Mirza S BaigDiscipline of Biosciences and Biomedical Engineering (BSBE), Indian Institute of Technology Indore (IITI), Simrol, 453552, India. msb@iiti.ac.in.ORCID http://orcid.org/0000-0001-8292-7130
Anjali RoyDiscipline of Biosciences and Biomedical Engineering (BSBE), Indian Institute of Technology Indore (IITI), Simrol, 453552, India.
Sajjan RajpootDiscipline of Biosciences and Biomedical Engineering (BSBE), Indian Institute of Technology Indore (IITI), Simrol, 453552, India.
Dongfang LiuDepartment of Pathology, Immunology and Laboratory Medicine, Rutgers University-New Jersey Medical School, 185 South Orange Avenue, Newark, NJ, 07103, USA.
Rajkumar SavaiMax Planck Institute for Heart and Lung Research, Member of the German Center for Lung Research (DZL), Member of the Cardio-Pulmonary Institute (CPI), 61231, Bad Nauheim, Germany.
Sreeparna BanerjeeDepartment of Biological Sciences, Middle East Technical University (METU), Ankara, 06800, Turkey.
Manabu KawadaLaboratory of Oncology, Institute of Microbial Chemistry (BIKAKEN), 3-14-23 Kamiosaki, Shinagawa-ku, Tokyo, 141-0021, Japan.
Syed M FaisalNational Institute of Animal Biotechnology (NIAB), Hyderabad, 500032, India.
Rohit SalujaDepartment of Biochemistry, All India Institute of Medical Sciences (AIIMS), Bhopal, 462020, India.
Uzma SaqibDiscipline of Chemistry, Indian Institute of Technology Indore (IITI), Simrol, 453552, India.
Tomokazu OhishiLaboratory of Oncology, Institute of Microbial Chemistry (BIKAKEN), 3-14-23 Kamiosaki, Shinagawa-ku, Tokyo, 141-0021, Japan.
Kishore K WaryDepartment of Pharmacology, The University of Illinois at Chicago, Chicago, IL, 60612, USA. kkwary@uic.edu.
Indian Institute of Technology Indore · INMicrobial Chemistry Research Foundation · JPAll India Institute of Medical Sciences Bhopal · INJustus-Liebig-Universität Gießen · DEMiddle East Technical University · TRNational Institute of Animal Biotechnology · INRutgers, The State University of New Jersey · USUniversity of Illinois Chicago · US

Funding

Department of Biotechnology , Ministry of Science and Technology BT/RLF/Re-entry/26/2013Department of Science and Technology, Ministry of Science and Technology ECR/2016/00852Indian Institute of Technology MHRD
6 · The paper itself

Abstract

backgroundThis review focuses on exosomes derived from various cancer cells. The review discusses the possibility of differentiating macrophages in alternatively activated anti-inflammatory pro-tumorigenic M2 macrophage phenotypes and classically activated pro-inflammatory, anti-tumorigenic M1 macrophage phenotypes in the tumor microenvironment (TME). The review is divided into two main parts, as follows: (1) role of exosomes in alternatively activating M2-like macrophages-breast cancer-derived exosomes, hepatocellular carcinoma (HCC) cell-derived exosomes, lung cancer-derived exosomes, prostate cancer-derived exosomes, Oral squamous cell carcinoma (OSCC)-derived exosomes, epithelial ovarian cancer (EOC)-derived exosomes, Glioblastoma (GBM) cell-derived exosomes, and colorectal cancer-derived exosomes, (2) role of exosomes in classically activating M1-like macrophages, oral squamous cell carcinoma-derived exosomes, breast cancer-derived exosomes, Pancreatic-cancer derived modified exosomes, and colorectal cancer-derived exosomes, and (3) exosomes and antibody-dependent cellular cytotoxicity (ADCC). This review addresses the following subjects: (1) crosstalk between cancer-derived exosomes and recipient macrophages, (2) the role of cancer-derived exosome payload(s) in modulating macrophage fate of differentiation, and (3) intracellular signaling mechanisms in macrophages regarding the exosome's payload(s) upon its uptake and regulation of the TME. EVIDENCE: Under the electron microscope, nanoscale exosomes appear as specialized membranous vesicles that emerge from the endocytic cellular compartments. Exosomes harbor proteins, growth factors, cytokines, lipids, miRNA, mRNA, and DNAs. Exosomes are released by many cell types, including reticulocytes, dendritic cells, B-lymphocytes, platelets, mast cells, and tumor cells. It is becoming clear that exosomes can impinge upon signal transduction pathways, serve as a mediator of signaling crosstalk, thereby regulating cell-to-cell wireless communications.

conclusionBased on the vesicular cargo, the molecular constituents, the exosomes have the potential to change the fate of macrophage phenotypes, either M1, classically activated macrophages, or M2, alternatively activated macrophages. In this review, we discuss and describe the ability of tumor-derived exosomes in the mechanism of macrophage activation and polarization.

Indexed as

AnimalsExosomesHumansMacrophagesNeoplasmsPhenotypeExosomesInflammatory responseM1 macrophagesM2 macrophagesTumor

Identifiers

PMID32162012
OpenAlexW3011299571

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.