Evidence map›Paper›PMID 41015590›Full record

ReviewNaunyn-Schmiedeberg's archives of pharmacology2026

CAF-derived exosomes: orchestrators of dysregulated signaling pathways in breast cancer progression.

Almuthana K Hameed, Safia Obaidur Rab, Thanaa Amir Ahmed, Muktesh Chandra, Jaafaru Sani Mohammed, Renukajyothi S, Priya Priyadarshini Nayak, Prakhar Tomar, Ahmed Hussn, Abbas Fadhel Ali

Abstract readReview
PubMed Publisher
In one paragraph

Review in Naunyn-Schmiedeberg's archives of pharmacology, 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

10 authors.

Almuthana K HameedDepartment of Medical Physics, College of Applied Sciences-Heet, University of Anbar, Ramadi, Al Anbar, 31001, Iraq. almuthana.khamees@uoanbar.edu.iq.ORCID http://orcid.org/0009-0005-4949-1810
Safia Obaidur RabDepartment of Clinical Laboratory Sciences, College of Applied Medical Sciences, King Khalid University, Abha, Saudi Arabia.
Thanaa Amir AhmedCollege of Nursing, University of Al Maarif, Ramadi, Al Anbar, 31001, Iraq. thana.amir@uoa.edu.iq.ORCID http://orcid.org/0009-0004-5535-3935
Muktesh ChandraMarwadi University Research Center, Department of Bioinformatics, Faculty of Engineering & Technology, Marwadi University, Rajkot, Gujarat, India.
Jaafaru Sani MohammedMedical Analysis Department, Faculty of Applied Science, Tishk International University, Erbil, Iraq.ORCID http://orcid.org/0000-0002-6635-4931
Renukajyothi SDepartment of Biotechnology and Genetics, School of Sciences, JAIN (Deemed to Be University), Bangalore, Karnataka, India.
Priya Priyadarshini NayakDepartment of Medical Oncology, IMS And SUM Hospital, Siksha ‛O' Anusandhan (Deemed to Be University), Bhubaneswar, Odisha, 751003, India.ORCID http://orcid.org/0009-0001-8421-3630
Prakhar TomarCentre for Research Impact and Outcome, Chitkara University Institute of Engineering and Technology, Chitkara University, Rajpura, Punjab, 140401, India.
Ahmed HussnDepartment of Medical Analysis, Medical Laboratory Technique College, The Islamic University, Najaf, Iraq.
Abbas Fadhel AliDepartment of Medical Laboratories Technology, AL-Nisour University College, Baghdad, Iraq.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer-associated fibroblasts (CAFs) play a pivotal role in breast cancer (BC) progression by modulating the tumor microenvironment through exosome-mediated interactions. CAF-derived exosomes are rich in bioactive molecules such as metabolites, proteins, and non-coding RNAs that influence metabolic reprogramming in BC cells. These exosomes facilitate the transfer of metabolic enzymes and signaling molecules that enhance glycolysis, lipid metabolism, and oxidative phosphorylation, thereby supporting tumor growth, therapy resistance, and metastasis. This review highlights the molecular mechanisms underlying the role of CAF-derived exosomes in BC metabolism, with a focus on their contributions to metabolic plasticity and tumor progression. Potential therapeutic strategies targeting CAF exosome biogenesis, release, or uptake will also be discussed to shed light on innovative approaches for disrupting this metabolic symbiosis.

Indexed as

Breast NeoplasmsCancer-Associated FibroblastsExosomesAnimalsDisease ProgressionFemaleHumansSignal TransductionTumor MicroenvironmentBreast cancerCancer-associated fibroblastsExosomesTumor microenvironment

Identifiers

PMID41015590

What Socratic 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 Socratic graph.