Evidence map›Paper›PMID 33234577›Full record

ArticleMolecular cancer research : MCR2021

Multiorgan Signaling Mobilizes Tumor-Associated Erythroid Cells Expressing Immune Checkpoint Molecules.

Yasuyo Sano, Toshimi Yoshida, Min-Kyung Choo, Yanek Jiménez-Andrade, Kathryn R Hill, Katia Georgopoulos, Jin Mo Park

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.0field-weighted citation impact, top 11% 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

23 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  7. ST2Clinical and translational allergy · 2025
    Article
  8. Article
  9. Article
  10. Review
  11. Immunoregulation role of the erythroid cells.Frontiers in immunology · 2024
    Review
  12. Review
  13. Erythroid Cells as Full Participants in the Tumor Microenvironment.International journal of molecular sciences · 2023
    Review
  14. Review
  15. Tumor-associated myeloid cells in cancer immunotherapy.Journal of hematology & oncology · 2023
    Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 2 countries.

Yasuyo SanoCutaneous Biology Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts.
Toshimi YoshidaCutaneous Biology Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts.
Min-Kyung ChooCutaneous Biology Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts.
Yanek Jiménez-AndradeCutaneous Biology Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts.ORCID https://orcid.org/0000-0002-8066-0169
Kathryn R HillCutaneous Biology Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts.ORCID https://orcid.org/0000-0003-4190-7808
Katia GeorgopoulosCutaneous Biology Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts.
Jin Mo ParkCutaneous Biology Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts. jmpark@cbrc2.mgh.harvard.edu.
Massachusetts General Hospital · US

Funding

Ikaros regulation: Study on hemolymphopoiesisR01HL140622 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI KATIA GEORGOPOULOS · 2017 to 2026
$6.1M
Erythropoietin receptor-driven tumor initiation and progressionR01CA182405 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI PARK, JIN MO · 2014 to 2018
$1.7M
NCI NIH HHS R01 CA182405NHLBI NIH HHS R01 HL140622
6 · The paper itself

Abstract

Hematopoietic-derived cells are integral components of the tumor microenvironment and serve as critical mediators of tumor-host interactions. Host cells derived from myeloid and lymphoid lineages perform well-established functions linked to cancer development, progression, and response to therapy. It is unclear whether host erythroid cells also contribute to shaping the path that cancer can take, but emerging evidence points to this possibility. Here, we show that tumor-promoting environmental stress and tumor-induced hemodynamic changes trigger renal erythropoietin production and erythropoietin-dependent expansion of splenic erythroid cell populations in mice. These erythroid cells display molecular features indicative of an immature erythroid phenotype, such as the expression of both CD71 and TER119 and the retention of intact nuclei, and express genes encoding immune checkpoint molecules. Nucleated erythroid cells with similar properties are present in mouse and human tumor tissues. Antibody-mediated erythropoietin blockade reduces tumor-responsive erythroid cell induction and tumor growth. These findings reveal the potential of tumor-induced erythropoietin and erythroid cells as targets for cancer treatment. IMPLICATIONS: : Our study identifies erythropoietin and erythroid cells as novel players in tumor-host interactions and highlights the involvement of multiorgan signaling events in their induction in response to environmental stress and tumor growth.

Indexed as

AnimalsCell DifferentiationErythroid CellsHumansImmune Checkpoint ProteinsMiceSignal TransductionImmune Checkpoint Proteins

Identifiers

PMID33234577
PMCPMC7925379
OpenAlexW3108501667

What OpenQuestion holds

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Registered trials

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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.