ReviewMedical oncology (Northwood, London, England)2025
Macrophage-cancer cell crosstalk in breast cancer chemotherapy resistance.
Review in Medical oncology (Northwood, London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Partial FAK suppression promotes tumor growth, an effect reversed by macrophage p110δ PI3K inactivation.Molecular oncology · 2026Article
- Isolation and Characterization of Glycosylated Fatty Acid Amides from the Norwegian Deep-Sea SpongeMarine drugs · 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
10 authors.
Funding
Abstract
Breast cancer (BC) represents one of the most prevalent malignancies in the female population and constitutes a leading cause of cancer-associated mortality among women globally. The emergence of chemoresistance persists as a critical challenge in current breast cancer therapeutic strategies. Malignant tumors are enveloped by a sophisticated assemblage of cellular and non-cellular components that collectively establish the tumor microenvironment (TME). Notably, tumor-associated macrophages (TAMs), being one of the most abundant immune infiltrates within the TME, have been demonstrated to play an instrumental role in the development and progression of chemotherapeutic resistance mechanisms. Recent studies have revealed that TAMs and breast cancer cells engage in complex bidirectional interactions. This crosstalk not only facilitates tumor immune evasion but also promotes chemotherapy resistance in breast cancer through the secretion of various cytokines, chemokines, growth factors, and other bioactive molecules. Therefore, elucidating the underlying mechanisms by which TAMs contribute to chemotherapy resistance is of significant importance. This review summarizes the dynamic and bidirectional regulatory network formed between TAMs and BC. Centering on this network, it comprehensively analyzes the molecular mechanisms by which TAMs regulate chemotherapy resistance in BC, summarizes potential targeted drugs that disrupt molecular interactions between TAMs and BC, and discusses the therapeutic prospects of combining these drugs with chemotherapy and immunotherapy. The findings aim to provide novel insights into potential molecular targets for overcoming chemotherapy resistance and to explore new therapeutic strategies for breast cancer patients.
Indexed as
Identifiers
41441951What OpenQuestion 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 OpenQuestion graph.