ReviewBreast cancer research : BCR2025
Macrophages in obesity-related breast cancer: mechanistic insights and therapeutic opportunities.
Review in Breast cancer research : BCR, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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.
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.
Who cites it
4 citing papers in PubMed.
- Review
- Understanding the Interplay Between Obesity and Cancer: From Mechanisms to Therapeutic Opportunities.Cancers · 2026Review
- Breast Cancer Milieu Maneuvers Cancer-Associated Macrophages to Synergize Neoplastic Repertoires.Cancers · 2026Review
- DXA-Derived Visceral and Subcutaneous Adipose Tissue and Postmenopausal Breast Cancer Mortality.Current oncology (Toronto, Ont.) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Obesity has emerged as a global public health crisis, significantly increasing susceptibility to malignancies, including breast cancer. In the context of Obesity-Related Breast Cancer (ORBC), the abundant adipose tissue in the mammary gland profoundly reshapes the tumor microenvironment (TME). Whereas obesity drives chronic, low-grade inflammation through pro-inflammatory M1 adipose tissue macrophages (ATMs), tumor-associated macrophages (TAMs) acquire a predominantly immunosuppressive M2 phenotype that promotes angiogenesis, immune evasion, and treatment resistance. This review examines macrophage ontogeny, polarization, and functional heterogeneity in ORBC, highlighting how obesity-induced cytokines (e.g. TNF-α, IL-6), reactive oxygen species, and metabolic reprogramming collectively reshape the TME to foster tumor initiation, progression, and metastasis. We further evaluate emerging therapeutic strategies—such as CSF-1R inhibitors, PD-1/PD-L1 checkpoint blockade, and CAR-macrophage immunotherapies—that target macrophages recruitment, polarization, and immunometabolic pathways in ORBC.
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What Socratic holds
Registered trials
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.