Evidence map›Paper›PMID 42291185›Full record

ArticleiScience2026

Stromal peroxidasin drives early tumor growth in breast cancer.

Kaitlin Wyllie, Ellie T Y Mok, Que Emmi Tran, Elysse C Filipe, Jessica L Chitty, Ron Enriquez, Anaiis Zaratzian, Andrew M Da Silva, Michael Tayao, David Gallego-Ortega and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

14 authors.

Kaitlin WyllieThe Garvan Institute of Medical Research and The Kinghorn Cancer Centre, Sydney, NSW, Australia.
Ellie T Y MokThe Garvan Institute of Medical Research and The Kinghorn Cancer Centre, Sydney, NSW, Australia.
Que Emmi TranThe Garvan Institute of Medical Research and The Kinghorn Cancer Centre, Sydney, NSW, Australia.
Elysse C FilipeThe Garvan Institute of Medical Research and The Kinghorn Cancer Centre, Sydney, NSW, Australia.
Jessica L ChittyThe Garvan Institute of Medical Research and The Kinghorn Cancer Centre, Sydney, NSW, Australia.
Ron EnriquezThe Garvan Institute of Medical Research and The Kinghorn Cancer Centre, Sydney, NSW, Australia.
Anaiis ZaratzianThe Garvan Institute of Medical Research and The Kinghorn Cancer Centre, Sydney, NSW, Australia.
Andrew M Da SilvaThe Garvan Institute of Medical Research and The Kinghorn Cancer Centre, Sydney, NSW, Australia.
Michael TayaoThe Garvan Institute of Medical Research and The Kinghorn Cancer Centre, Sydney, NSW, Australia.
David Gallego-OrtegaSchool of Biomedical Engineering, University of Technology, Sydney, NSW, Australia.
Sandra O'TooleThe Garvan Institute of Medical Research and The Kinghorn Cancer Centre, Sydney, NSW, Australia.
Amelia L ParkerThe Garvan Institute of Medical Research and The Kinghorn Cancer Centre, Sydney, NSW, Australia.
Vasilios PanagopoulosCentre for Cancer Biology, College of Health, Adelaide University, Adelaide, SA, Australia.
Thomas R CoxThe Garvan Institute of Medical Research and The Kinghorn Cancer Centre, Sydney, NSW, Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The extracellular matrix (ECM) plays multifaceted tumor-promoting and tumor-restraining roles in breast cancer progression. Extracellular peroxidases represent a critical yet underexplored component of stromal remodeling machinery. Peroxidasin (PXDN), an extracellular peroxidase with established roles in collagen IV crosslinking, has been associated with poor outcomes in several cancers, but its role in breast cancer remains unclear. Through temporal proteomic analysis of dysregulated ECM proteins, we identified PXDN as upregulated during early tumor development in mouse models. In human breast cancers, PXDN expression shows compartment-specific associations with patient outcome, with high stromal PXDN, predominantly cancer-associated fibroblast (CAF)-derived, correlating with poor prognosis. We demonstrate that PXDN regulates CAF behavior, with subsequent matrix remodeling affecting cancer cell behavior. Reduction of CAF-derived PXDN

Indexed as

cancer systems biologycell biologymolecular biology

Identifiers

PMID42291185
PMCPMC13253085

What OpenQuestion 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 OpenQuestion graph.