Evidence map›Paper›PMID 33230244›Full record

ArticleOncogene2021

Monocytic and granulocytic myeloid-derived suppressor cell plasticity and differentiation are organ-specific.

Prajna Guha, Jillian Gardell, Benjamin Rabinowitz, Mikayla Lopes, Nicholas A DaSilva, David Rowley, Steven C Katz

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

22 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Reprogramming the neuroblastoma tumor immune microenvironment to enhance GPC2 CAR T cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
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  13. The tumor-immune ecosystem in shaping metastasis.American journal of physiology. Cell physiology · 2023
    Review
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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.

Prajna GuhaRoger Williams Medical Center, Immuno-oncology Institute and Department of Medicine Immunotherapy Service, Providence, RI, USA.
Jillian GardellRoger Williams Medical Center, Immuno-oncology Institute and Department of Medicine Immunotherapy Service, Providence, RI, USA.
Benjamin RabinowitzRoger Williams Medical Center, Immuno-oncology Institute and Department of Medicine Immunotherapy Service, Providence, RI, USA.
Mikayla LopesRoger Williams Medical Center, Immuno-oncology Institute and Department of Medicine Immunotherapy Service, Providence, RI, USA.
Nicholas A DaSilvaDepartment of Biomedical and Pharmaceutical Sciences, University of Rhode Island, Kingston, RI, USA.
David RowleyDepartment of Biomedical and Pharmaceutical Sciences, University of Rhode Island, Kingston, RI, USA.ORCID http://orcid.org/0000-0001-7808-1312
Steven C KatzRoger Williams Medical Center, Immuno-oncology Institute and Department of Medicine Immunotherapy Service, Providence, RI, USA. skatz@chartercare.org.ORCID http://orcid.org/0000-0002-6030-9312
Roger Williams Medical Center · USBoston University · USUniversity of Rhode Island · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myeloid-derived suppressor cells (MDSCs) are a heterogeneous population of immature myeloid cells that proliferate in the setting of cancer and have potent immunosuppressive functions hindering anti-tumor immunity. Here we establish that the immunologic landscape and tumor microenvironments (TME) vary between different organs which discretely shape MDSC repertoires. We found that pSTAT3 signaling exerts a dominant effect on MDSC programming in liver metastasis (LM). In contrast, in lung metastasis (LuM), MDSC programming is driven mainly by pSTAT5. Adoptive transfer of LM-MDSC into LuM resulted in a shift from pSTAT3 signaling to pSTAT5, in association with an overall shift toward lung MDSC programming. A shift from more immunosuppressive M-MDSC to G-MDSC, along with enhanced differentiation of MDSCs into pro-inflammatory M1 macrophages in LuM, indicated that MDSC plasticity and differentiation patterns are environmentally dependent. Using mass spectroscopy, we confirmed that LM-MDSCs showed enhanced expression of key proliferation pathway markers. This confirmed that liver-specific MDSC programing was comprehensive but reversible, implying that therapeutic targeting of LM-MDSC could prime the TME in a favorable manner. Our data suggest that MDSC programming in response to malignancy is highly dependent on organ-specific conditions and is modifiable.

Indexed as

Tumor MicroenvironmentAnimalsCell Line, TumorGranulocytesLung NeoplasmsMaleMiceMonocytesMyeloid-Derived Suppressor CellsOrgan Specificity

Identifiers

PMID33230244
OpenAlexW3109558738

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.