Evidence map›Paper›PMID 41991755›Full record

ArticleBreast cancer research and treatment2026

In vivo exposure to CXCL12-high CAFs and chronic CXCL12 stimulation in vitro is sufficient to enhance metastasis of ER-positive breast cancer.

Philip C Miller, Utsav Sharma, JiaXiang Tao, Jun Sun, Kelsie Medina-Saenz, Manuel Picon-Ruiz, Cynthia Morata-Tarifa, Susan M Bare, Joyce M Slingerland, Dorraya El-Ashry and 1 more

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Article in Breast cancer research and treatment, 2026. 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

11 authors.

Philip C Miller *Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC, USA.
Utsav Sharma *Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC, USA.
JiaXiang TaoDepartment of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC, USA.
Jun SunSylvester Comprehensive Cancer Center, University of Miami, Miller School of Medicine, Miami, FL, USA.
Kelsie Medina-SaenzDepartment of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC, USA.
Manuel Picon-RuizSylvester Comprehensive Cancer Center, University of Miami, Miller School of Medicine, Miami, FL, USA.
Cynthia Morata-TarifaSylvester Comprehensive Cancer Center, University of Miami, Miller School of Medicine, Miami, FL, USA.
Susan M BareDepartment of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC, USA.
Joyce M SlingerlandDepartment of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC, USA.
Dorraya El-AshryDepartment of Laboratory Medicine and Pathology, Masonic Cancer Center, University of Minnesota, Minneapolis, MN, USA. mel316@georgetown.edu.
Marc E LippmanDepartment of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC, USA.

Funding

Breast Cancer Research Foundation, United States BCRF-18-099
6 · The paper itself

Abstract

purposeCancer-associated fibroblasts (CAFs) play important roles in breast cancer (BC) progression and metastasis. Here we investigated whether CAFs from indolent vs. aggressive BCs differ in gene expression profiles and how they impact metastasis. EXPERIMENTAL

designGenotypic differences in CAF lines from basal-like (CAF23

resultsCo-injection of MCF7 with CAF23

conclusionsThese findings suggest that CXCL12 overexpressing CAFs can induce gene expression changes in breast cancer that promote breast cancer metastasis, potentially through expansion of the CSC population. Targeting the CAF CXCL12/CXCR4 axis may offer a novel treatment strategy for metastatic breast cancer and warrants further investigation. STATEMENT OF TRANSLATIONAL RELEVANCE: Cancer associated fibroblasts (CAF) within the breast tumor microenvironment influence breast cancer behavior. Our study indicates that high CXCL12-expressing CAFs can induce a stable metastatic phenotype in estrogen receptor positive breast cancer models. Gene expression similarities between a high CXCL12 CAF line and high CXCL12-expressing CAFs from primary and metastatic human breast cancers define a CXCL12-high CAF signature that is prognostic of poor BC patient outcome. Furthermore, gene expression changes induced in MCF7 cells by CXCL12 high CAFs in vivo were similar to the gene expression differences between normal and malignant breast epithelial cells in breast cancers containing CXCL12 high CAFs. Disruption of CAF-driven, CXCL12-mediated reprogramming of breast cancer cells might provide an opportunity to prevent or treat breast cancer metastasis.

Indexed as

Breast NeoplasmsCancer-Associated FibroblastsChemokine CXCL12Receptors, EstrogenAnimalsCell Line, TumorEpithelial-Mesenchymal TransitionFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMCF-7 CellsMiceNeoplasm MetastasisNeoplastic Stem CellsPrognosisChemokine CXCL12CXCL12 protein, humanReceptors, EstrogenCancer associated fibroblastCXCL12ER positiveMetastasisSDF1Xenograft

Identifiers

PMID41991755

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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.