Evidence map›Paper›PMID 42196611›Full record

ReviewInternational journal of molecular sciences2026

CAFs and Endocrine Therapy Resistance in Hormone Receptor-Positive Breast Cancer.

Amalia A Sofianidi, Vaia K Stafyla, Flora Zagouri

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 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

3 authors.

Amalia A SofianidiOncology Unit, Aretaieion University Hospital, School of Medicine, National and Kapodistrian University of Athens, 11527 Athens, Greece.ORCID 0009-0005-9882-9478
Vaia K Stafyla4th Department of Surgery, Attiko Hospital, School of Medicine, National and Kapodistrian University of Athens, 12462 Athens, Greece.
Flora ZagouriOncology Unit, Aretaieion University Hospital, School of Medicine, National and Kapodistrian University of Athens, 11527 Athens, Greece.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The development of endocrine resistance represents a major obstacle when treating hormone receptor-positive breast cancer. The tumor microenvironment (TME), represented by cancer-associated fibroblasts (CAFs) in this context, has recently been proposed as a key mediator significantly contributing to resistance against currently available endocrine therapies. The exact mechanisms behind this interaction are not fully understood; specific breast CAF subtypes have been linked to it, such as CAFs lacking the expression of the glycoprotein CD146 or maintaining the expression of CD63. Other proposed mechanisms include signaling pathways aberrantly activated in CAFs, epigenetic modifications mainly in the form of long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), and paracrine signaling, all limiting endocrine modulation effectiveness. Strategies aiming to simultaneously target CAFs and endocrine signaling in luminal breast cancer are currently being developed. Fibroblast growth factor receptor (FGFR) targeting in combination with endocrine inhibition has already entered the clinical trial landscape. However, CAFs are a highly diverse and heterogeneous cell population, making their targeting complex and difficult to implement in clinical practice.

Indexed as

Antineoplastic Agents, HormonalBreast NeoplasmsCancer-Associated FibroblastsDrug Resistance, NeoplasmAnimalsFemaleGene Expression Regulation, NeoplasticHumansReceptors, EstrogenSignal TransductionTumor MicroenvironmentAntineoplastic Agents, HormonalReceptors, Estrogenbreast cancerCAFscancer-associated fibroblastsendocrine resistanceluminal

Identifiers

PMID42196611
PMCPMC13207922

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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.