Evidence map›Paper›PMID 41518488›Full record

ArticleBiotechnology and bioengineering2026

Dynamic Immune Cell Composition, Phenotypes, and Signaling in an Engineered Metastatic Niche.

Rebecca S Pereles, Jyotirmoy Roy, Michael D Brooks, Max S Wicha, Jacqueline S Jeruss, Lonnie D Shea, Sophia M Orbach

Abstract read
In one paragraph

Article in Biotechnology and bioengineering, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

7 authors.

Rebecca S PerelesDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, Michigan, USA.
Jyotirmoy RoyDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, Michigan, USA.
Michael D BrooksDepartment of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Max S WichaDepartment of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Jacqueline S JerussDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, Michigan, USA.
Lonnie D SheaDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, Michigan, USA.ORCID https://orcid.org/0000-0002-9296-9673
Sophia M OrbachDepartment of Biomedical Engineering, Rowan University, Glassboro, New Jersey, USA.

Funding

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 CA243421The Dynami Foundation, the Breast Cancer Research Foundation BCRF-18-173The National Institutes of Health (L.D.S., J.S.J., and M.S.W.) R01CA214384The National Institutes of Health (L.D.S., J.S.J., and M.S.W.) R01CA243916The National Institutes of Health (L.D.S., J.S.J., and M.S.W.) R35CA197585The UM Postdoctoral Translational Scholar Program and NRSA F32CA243421
6 · The paper itself

Abstract

In breast cancer patients, metastasis is the stage of disease where prognosis significantly worsens. However, the timing at which metastasis initiates and the location of metastatic lesions in an organ are stochastic, limiting the timely identification of disease and the administration of treatments. Herein, we employ a synthetic metastatic niche comprised of a microporous scaffold to investigate the dynamic immune processes associated with metastatic progression. Upon implantation, the porous scaffold is infiltrated with immune cells and recruits tumor cells. We have previously reported stable tumor cell numbers in the scaffold, suggesting a state of metastatic dormancy. Towards understanding dormancy, we investigated the immune cell dynamics at the scaffold, including neutrophils, monocytes, and dendritic cells, and compared these changes to the lungs, the native metastatic niche in this model. The cell phenotypes within the scaffold microenvironment are initially polarized toward an anti-tumor phenotype and become progressively more pro-tumor with disease progression, similar to the lung microenvironment. However, the phenotypes at the scaffold are consistently less pro-tumor than the phenotypes in the lung, consistent with the lung supporting tumor cell expansion and the scaffold exhibiting dormancy. Signaling pathways identified from the analysis are consistent with the changing innate cell phenotypes, with macrophages having a significant role during the early responses and neutrophils dominating the latter stages of disease. Collectively, the scaffold captures the immune dynamics during disease progression and the signaling that underlies stable tumor cell numbers, providing a tool for investigating the mechanisms of disease progression.

Indexed as

Breast NeoplasmsNeoplasm MetastasisSignal TransductionTissue ScaffoldsTumor MicroenvironmentAnimalsFemaleHumansPhenotypecell phenotypescell signalingimmune cellsmetastasissynthetic metastatic niches

Identifiers

PMID41518488
PMCPMC13003427

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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.