Evidence map›Paper›PMID 40590919›Full record

ReviewNaunyn-Schmiedeberg's archives of pharmacology2025

Targeting CAF-specific metabolic pathways in breast cancer.

Alaa Khalaf Bediwi, Ahmed Hjazi, Mundher Kedhem, Ali G Alkhathami, RenukaJyothi S, Priya Priyadarshini Nayak, Amrita Pargaien, Udaybir Singh, Fathi Jihad Hammady, Salah Abdulhadi Salih

Abstract readReview
PubMed Publisher
In one paragraph

Review in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

10 authors.

Alaa Khalaf BediwiMedical Laboratory Techniques Department, College of Health and Medical Technology, University of Al-Maarif, Anbar, Ramadi, Iraq.
Ahmed HjaziDepartment of Medical Laboratory, College of Applied Medical Sciences, Prince Sattam Bin Abdulaziz University, 11942, Al-Kharj, Saudi Arabia. hjaziahmed703@gmail.com.ORCID 0000-0002-1129-6930
Mundher KedhemCollege of Pharmacy, The Islamic University, Najaf, Iraq.
Ali G AlkhathamiDepartment of Clinical Laboratory Sciences, College of Applied Medical Sciences, King Khalid University, Abha, Saudi Arabia.
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 0009-0001-8421-3630
Amrita PargaienDepartment of Pharmacy, Graphic Era Hill University, Bhimtal, Uttarakhand, India.
Udaybir SinghCentre for Research Impact & Outcome, Chitkara University Institute of Engineering and Technology, Chitkara University, Rajpura, 140401, Punjab, India.
Fathi Jihad HammadyDepartment of Medical Laboratories Technology, Mazaya University College, Nasiriyah, Iraq.
Salah Abdulhadi SalihDepartment of Medical Laboratories Technology, Al-Nisour University College, Baghdad, Iraq.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer (BC) cells are distinguished by their capacity to reconfigure metabolism to support rapid growth and survive in hypoxic, nutrient-deficient environments. In the breast tumor microenvironment (TME), metabolic changes-including the Warburg effect, modifications in Krebs cycle intermediates, and adjusted oxidative phosphorylation-are closely associated with the dynamic signaling between tumor cells and stromal elements. Cancer-associated fibroblasts (CAFs), a diverse and adaptable group inside the stroma, significantly influence metabolic pathways, including those regulating glucose, amino acid, and lipid metabolism. Recent research underscores that the metabolic interaction between BC cells and CAFs not only promotes tumor growth and invasion but also facilitates treatment resistance. This review is aimed at consolidating the existing data on the metabolic interactions between BC cells and CAFs, highlighting molecular mechanisms and pathways that could represent potential targets for future therapies.

Indexed as

Antineoplastic AgentsBreast NeoplasmsCancer-Associated FibroblastsAnimalsFemaleHumansMetabolic Networks and PathwaysTumor MicroenvironmentAntineoplastic AgentsBreast cancerCancer-associated fibroblastsMetabolic pathwaysTargeted therapyTumor microenvironment

Identifiers

PMID40590919

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.