Evidence map›Paper›PMID 33669537›Full record

ReviewCancers2021

Tumor Immune Evasion Induced by Dysregulation of Erythroid Progenitor Cells Development.

Tomasz M Grzywa, Magdalena Justyniarska, Dominika Nowis, Jakub Golab

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

25 citing papers in PubMed, 37 citations in OpenAlex.

  1. Acute-on-chronic liver failure-associated CD45Cellular and molecular life sciences : CMLS · 2026
    Article
  2. Review
  3. Article
  4. Insights into the mechanisms of angiogenesis in hepatoblastoma.Frontiers in cell and developmental biology · 2025
    Review
  5. Review
  6. Article
  7. Importance of CD71Journal of clinical laboratory analysis · 2024
    Article
  8. Review
  9. Immunoregulation role of the erythroid cells.Frontiers in immunology · 2024
    Review
  10. Review
  11. CD45Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2023
    Article
  12. Article
  13. Erythroid Cells as Full Participants in the Tumor Microenvironment.International journal of molecular sciences · 2023
    Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. 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

4 authors at 1 institution in 1 country.

Tomasz M GrzywaDepartment of Immunology, Medical University of Warsaw, 02-097 Warsaw, Poland.ORCID 0000-0002-1809-248X
Magdalena JustyniarskaDepartment of Immunology, Medical University of Warsaw, 02-097 Warsaw, Poland.
Dominika NowisLaboratory of Experimental Medicine, Medical University of Warsaw, 02-097 Warsaw, Poland.
Jakub GolabDepartment of Immunology, Medical University of Warsaw, 02-097 Warsaw, Poland.
Medical University of Warsaw · PL

Funding

Ministerstwo Nauki i Szkolnictwa Wyższego iONKO (Regionalna Inicjatywa Doskonalosci)Narodowe Centrum Nauki UMO-2019/35/B/NZ6/00540Warszawski Uniwersytet Medyczny 1M19/M/MG2/N/20
6 · The paper itself

Abstract

Cancer cells harness normal cells to facilitate tumor growth and metastasis. Within this complex network of interactions, the establishment and maintenance of immune evasion mechanisms are crucial for cancer progression. The escape from the immune surveillance results from multiple independent mechanisms. Recent studies revealed that besides well-described myeloid-derived suppressor cells (MDSCs), tumor-associated macrophages (TAMs) or regulatory T-cells (Tregs), erythroid progenitor cells (EPCs) play an important role in the regulation of immune response and tumor progression. EPCs are immature erythroid cells that differentiate into oxygen-transporting red blood cells. They expand in the extramedullary sites, including the spleen, as well as infiltrate tumors. EPCs in cancer produce reactive oxygen species (ROS), transforming growth factor β (TGF-β), interleukin-10 (IL-10) and express programmed death-ligand 1 (PD-L1) and potently suppress T-cells. Thus, EPCs regulate antitumor, antiviral, and antimicrobial immunity, leading to immune suppression. Moreover, EPCs promote tumor growth by the secretion of growth factors, including artemin. The expansion of EPCs in cancer is an effect of the dysregulation of erythropoiesis, leading to the differentiation arrest and enrichment of early-stage EPCs. Therefore, anemia treatment, targeting ineffective erythropoiesis, and the promotion of EPC differentiation are promising strategies to reduce cancer-induced immunosuppression and the tumor-promoting effects of EPCs.

Indexed as

anemiaCD71+ erythroid cellserythroid progenitor cellserythropoiesisimmune evasionineffective erythropoiesisTer-cells

Identifiers

PMID33669537
PMCPMC7922079
OpenAlexW3133034153

What Socratic 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 Socratic graph.