Evidence map›Paper›PMID 42120423›Full record

ArticleNature communications2026

E-cadherin inactivation shapes tumor microenvironment specificities in invasive lobular breast cancer.

Lounes Djerroudi, Rana Mhaidly, Yann Kieffer, Isabelle Damei, Hugo Croizer, Vithuzane Selvarasa, Geraldine Gentric, Laetitia Fuhrmann, Andreia Goncalves, Martial Caly and 13 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 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. Pitfalls in the Histological Diagnosis of Morphologic Variants of Invasive Lobular Carcinoma of the Breast.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2025
    Review
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

23 authors.

Lounes DjerroudiInstitut Curie, Stress and Cancer Laboratory, Equipe labélisée par la Ligue Nationale contre le Cancer, PSL Research University, Paris, France.ORCID http://orcid.org/0000-0002-5007-2964
Rana Mhaidly *Institut Curie, Stress and Cancer Laboratory, Equipe labélisée par la Ligue Nationale contre le Cancer, PSL Research University, Paris, France.
Yann Kieffer *Institut Curie, Stress and Cancer Laboratory, Equipe labélisée par la Ligue Nationale contre le Cancer, PSL Research University, Paris, France.ORCID http://orcid.org/0000-0003-2722-3071
Isabelle DameiInstitut Curie, Stress and Cancer Laboratory, Equipe labélisée par la Ligue Nationale contre le Cancer, PSL Research University, Paris, France.
Hugo CroizerInstitut Curie, Stress and Cancer Laboratory, Equipe labélisée par la Ligue Nationale contre le Cancer, PSL Research University, Paris, France.
Vithuzane SelvarasaInstitut Curie, Stress and Cancer Laboratory, Equipe labélisée par la Ligue Nationale contre le Cancer, PSL Research University, Paris, France.
Geraldine GentricInstitut Curie, Stress and Cancer Laboratory, Equipe labélisée par la Ligue Nationale contre le Cancer, PSL Research University, Paris, France.ORCID http://orcid.org/0000-0002-7558-8705
Laetitia FuhrmannInstitut Curie, Institute of Women's Cancer, Department of Diagnostic and Theragnostic Medicine, Paris, France.ORCID http://orcid.org/0000-0003-1755-6307
Andreia GoncalvesInstitut Curie, Institute of Women's Cancer, Department of Diagnostic and Theragnostic Medicine, Paris, France.
Martial CalyInstitut Curie, Institute of Women's Cancer, Department of Diagnostic and Theragnostic Medicine, Paris, France.
Camille RichardotInstitut Curie, Institute of Women's Cancer, Department of Diagnostic and Theragnostic Medicine, Paris, France.
Renaud LeclereInstitut Curie, Institute of Women's Cancer, Department of Diagnostic and Theragnostic Medicine, Paris, France.ORCID http://orcid.org/0000-0001-8737-6817
Enora LaasInstitut Curie, Institute of Women's Cancer, Department of Surgery, Paris Cedex 05, France.
Caroline MalhaireInstitut Curie, Institute of Women's Cancer, Department of Radiology, Paris Cedex 05, France.ORCID http://orcid.org/0000-0002-9235-9816
Kim CaoInstitut Curie, Institute of Women's Cancer, Department of Radiation Oncology, Paris Cedex 05, France.
Julia M HouthuijzenDivision of Molecular Pathology, Oncode Institute, The Netherlands Cancer Institute, Amsterdam, The Netherlands.ORCID http://orcid.org/0000-0003-0404-1961
Pim KloostermanDivision of Molecular Pathology, Oncode Institute, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Jos JonkersDivision of Molecular Pathology, Oncode Institute, The Netherlands Cancer Institute, Amsterdam, The Netherlands.ORCID http://orcid.org/0000-0002-9264-9792
Camille BenoistInstitut Curie, PSL University, Clinical Bioinformatics, Paris Cedex 05, France.
Victor RenaultInstitut Curie, PSL University, Clinical Bioinformatics, Paris Cedex 05, France.
François-Clément BidardInstitut Curie, Institute of Women's Cancer, Department of Medical Oncology, INSERM CIC 1428, Université Versailles Saint Quentin, Saint Cloud, France.ORCID http://orcid.org/0000-0001-5932-8949
Anne Vincent-SalomonInstitut Curie, Institute of Women's Cancer, Department of Diagnostic and Theragnostic Medicine, Paris, France. anne.salomon@curie.fr.ORCID http://orcid.org/0000-0001-5754-5771
Fatima Mechta-GrigoriouInstitut Curie, Stress and Cancer Laboratory, Equipe labélisée par la Ligue Nationale contre le Cancer, PSL Research University, Paris, France. fatima.mechta-grigoriou@curie.fr.ORCID http://orcid.org/0000-0002-3751-6989

Funding

Institut National de la Santé et de la Recherche Médicale (National Institute of Health and Medical Research) PC201317
6 · The paper itself

Abstract

Invasive lobular breast carcinoma (ILC) shows specific stromal features, and a high tumor-infiltrating lymphocyte (TIL) content being associated with poor patient prognosis. Here, we reveal the underlying mechanism by performing single-cell analysis, immunohistochemistry, deconvolution of bulk RNA-sequencing in a large female ILC series and functional assays. We show that E-cadherin (CDH1)-loss in breast cancer cells prevents differentiation of FAP+ inflammatory cancer-associated fibroblasts (iCAF) into FAP+ myofibroblastic CAF, leading to iCAF accumulation in ILC. In turn, FAP+ iCAF attract TILs into the tumor center, shaping their spatial organization. Subsequently, CDH1-inactivated ILC cancer cells promote immune escape through a lack of retention and activation of ITGAE-expressing resident memory CD8 + T lymphocytes (TRM). Hence, our study uncovers reciprocal interactions between CDH1-inactivated cancer cells, FAP+ iCAF and CD8 + TRM, providing insights into the ILC stromal reaction and revealing why and how TILs are associated with poor prognosis in ILC patients, a mechanism generalizable to other CDH1-inactivated cancer types.

Indexed as

Antigens, CDBreast NeoplasmsCadherinsCarcinoma, LobularTumor MicroenvironmentAnimalsCancer-Associated FibroblastsCD8-Positive T-LymphocytesCell DifferentiationCell Line, TumorEndopeptidasesFemaleFibroblast Activation Protein AlphaGelatinasesGene Expression Regulation, NeoplasticHumansAntigens, CDCadherinsCDH1 protein, humanEndopeptidasesFibroblast Activation Protein AlphaGelatinasesMembrane ProteinsSerine Endopeptidases

Identifiers

PMID42120423
PMCPMC13527148

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.