Evidence map›Paper›PMID 32878277›Full record

ReviewInternational journal of molecular sciences2020

Myeloid Cell Modulation by Tumor-Derived Extracellular Vesicles.

Ihor Arkhypov, Samantha Lasser, Vera Petrova, Rebekka Weber, Christopher Groth, Jochen Utikal, Peter Altevogt, Viktor Umansky

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

34 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Extracellular vesicles in spine tumors: biological roles, immune modulation, and therapeutic implications.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2026
    Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. 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

8 authors at 1 institution in 1 country.

Ihor ArkhypovSkin Cancer Unit, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany.
Samantha LasserSkin Cancer Unit, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany.
Vera PetrovaSkin Cancer Unit, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany.
Rebekka WeberSkin Cancer Unit, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany.
Christopher GrothSkin Cancer Unit, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany.
Jochen UtikalSkin Cancer Unit, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany.
Peter AltevogtSkin Cancer Unit, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany.
Viktor UmanskySkin Cancer Unit, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany.
German Cancer Research Center · DE

Funding

Bundesministerium für Bildung und Forschung SERPENTINE project in the ERA PerMed networkDeutsche Forschungsgemeinschaft 25933240/RTG 2099German Cancer Research Center CA181
6 · The paper itself

Abstract

Extracellular vesicles (EV) can carry proteins, RNA and DNA, thus serving as communication tools between cells. Tumor cells secrete EV, which can be taken up by surrounding cells in the tumor microenvironment as well as by cells in distant organs. Tumor-derived EV (TEV) contain factors induced by tumor-associated hypoxia such as heat shock proteins or a variety of microRNA (miRNA). The interaction of TEV with tumor and host cells can promote cancer angiogenesis, invasion and metastasis. Myeloid cells are widely presented in tissues, comprise the majority of immune cells and play an essential role in immune reactions and tissue remodeling. However, in cancer, the differentiation of myeloid cells and their functions are impaired, resulting in tumor promotion. Such alterations are due to chronic inflammatory conditions associated with cancer and are mediated by the tumor secretome, including TEV. A high capacity of myeloid cells to clear EV from circulation put them in the central position in EV-mediated formation of pre-metastatic niches. The exposure of myeloid cells to TEV could trigger numerous signaling pathways. Progenitors of myeloid cells alter their differentiation upon the contact with TEV, resulting in the generation of myeloid-derived suppressor cells (MDSC), inhibiting anti-tumor function of T and natural killer (NK) cells and promoting thereby tumor progression. Furthermore, TEV can augment MDSC immunosuppressive capacity. Different subsets of mature myeloid cells such as monocytes, macrophages, dendritic cells (DC) and granulocytes take up TEV and acquire a protumorigenic phenotype. However, the delivery of tumor antigens to DC by TEV was shown to enhance their immunostimulatory capacity. The present review will discuss a diverse and complex EV-mediated crosstalk between tumor and myeloid cells in the context of the tumor type, TEV-associated cargo molecules and type of recipient cells.

Indexed as

AnimalsCell DifferentiationExtracellular VesiclesHumansImmune ToleranceKiller Cells, NaturalMyeloid-Derived Suppressor CellsNeoplasmsTumor Microenvironmentcancerextracellular vesiclesimmunosuppressionmyeloid cells

Identifiers

PMID32878277
PMCPMC7504548
OpenAlexW3081946550

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.