ReviewDiscover oncology2026
MicroRNA-mediated modulation of cancer-associated fibroblasts in HER2-positive breast tumor microenvironment: a comprehensive review.
Review in Discover oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The intricate interplay within the tumor microenvironment (TME) significantly dictates the trajectory of cancer progression and therapeutic response. In HER2-positive breast cancer, a particularly aggressive subtype, cancer-associated fibroblasts (CAFs) emerge as pivotal stromal components, actively orchestrating malignant behaviors. Concurrently, microRNAs (miRNAs), small non-coding RNAs, serve as potent post-transcriptional regulators and critical mediators of intercellular communication, often encapsulated within exosomes. This review provides a comprehensive analysis of the reciprocal miRNA-mediated modulation between HER2-positive breast cancer cells and CAFs. It elucidates how tumor cell-derived miRNAs reprogram normal fibroblasts into pro-tumorigenic CAFs, and how CAF-derived miRNAs, in turn, influence HER2-positive cancer cell proliferation, invasion, metastasis, and crucially, resistance to HER2-targeted therapies. Understanding this dynamic axis reveals a self-sustaining feedback loop that drives disease advancement and therapeutic evasion. This synthesis underscores the immense potential of targeting these complex miRNA-CAF interactions as a novel strategy for diagnostic, prognostic, and therapeutic interventions, aiming to overcome the persistent challenge of resistance in HER2-positive breast cancer.
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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.