Evidence map›Paper›PMID 40269509›Full record

ArticleMolecular oncology2025

Early metastasis is characterized by Gr1+ cell dysregulation and is inhibited by immunomodulatory nanoparticles.

Jeffrey A Ma, Sophia M Orbach, Kate V Griffin, Kathryn Kang, Yining Zhang, Rebecca S Pereles, Ian A Schrack, Guillermo Escalona, Jacqueline S Jeruss, Lonnie D Shea

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

10 authors.

Jeffrey A MaDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI, USA.
Sophia M OrbachDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI, USA.
Kate V GriffinDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI, USA.
Kathryn KangDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI, USA.
Yining ZhangDepartment of Chemical Engineering, University of Michigan, Ann Arbor, MI, USA.
Rebecca S PerelesDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI, USA.
Ian A SchrackDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI, USA.
Guillermo EscalonaDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI, USA.
Jacqueline S JerussDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI, USA.
Lonnie D SheaDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI, USA.ORCID 0000-0002-9296-9673

Funding

XenograftP30CA046592 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Eric R. Fearon · 1988 to 2026
$178.2M
Nanoparticle-mediated reprogramming of circulating monocytes and neutrophils to decrease inflammation-mediated damage after traumaR01AI148076 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ANDERSON, AILEEN J, SHEA, LONNIE D · 2019 to 2023
$3.4M
Identifying intercellular circuits driving cell phenotypes within a nicheR01CA243916 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI JERUSS, JACQUELINE SARA, SHEA, LONNIE D · 2019 to 2023
$2.3M
Tissue engineering tools for monitoring the cellular and molecular response to therapyR01CA272940 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI JACQUELINE SARA JERUSS, Lonnie D Shea · 2023 to 2026
$1.7M
Heterogeneity of the Early Metastatic Niche in Cancer Progression and ChemoresistanceF32CA243421 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ORBACH, SOPHIA M · 2019 to 2021
$194k
NCI NIH HHS F32 CA243421NCI NIH HHS P30 CA046592NCI NIH HHS R01 CA243916NCI NIH HHS R01 CA272940NIAID NIH HHS R01 AI148076NIH HHS 1R01AI148076NIH HHS 1R01CA243916NIH HHS 1R01CA272940NIH HHS F32 CA243421
6 · The paper itself

Abstract

Cancer metastasis is supported by dysregulated myeloid-derived suppressor cells, but myeloid cells are highly heterogeneous populations with distinct subsets that may support or inhibit tumor cell colonization. We hypothesize that Gr1+ myeloid cells transform in phenotype to support tumor cell colonization at the metastatic niche. In the 4T1 model of metastatic breast cancer, we investigate changes in the composition and phenotype of Gr1+ cells between premetastatic disease and early metastasis. Gr1+ cells in the lung were found to transition towards immunosuppressive and tumor-supportive phenotypes with disease progression. While the composition of myeloid cells becomes dysregulated systemically, cells in the blood do not develop tumor-supportive phenotypes, indicating that protumor functions are specific to the lung. In vitro assays demonstrate that Gr1+ cells from early metastatic lungs support tumor cell survival, migration, and proliferation, which is linked to chitinase-3-like protein 1 (CHI3L1) signaling. The intravenous injection of polymeric nanoparticles reprograms Gr1+ cell phenotypes, reduces the secretion of CHI3L1, and inhibits metastasis. These findings indicate that dysregulated Gr1+ cells are a therapeutic target for early metastasis and can be targeted with polymeric nanoparticles.

Indexed as

ImmunomodulationLung NeoplasmsNanoparticlesReceptors, GlucocorticoidAnimalsBreast NeoplasmsCell Line, TumorCell MovementCell ProliferationFemaleHumansMiceMice, Inbred BALB CMyeloid CellsNeoplasm MetastasisReceptors, GlucocorticoidGr1+ myeloid cellsimmunosuppressionmetastatic nichemyeloid‐derived suppressor cellsnanoparticles

Identifiers

PMID40269509
PMCPMC12515690

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.