Evidence map›Paper›PMID 41186624›Full record

ReviewMolecular biology reports2025

Tumor microenvironment in breast cancer: cellular crosstalk, pathways, and therapeutic insights.

Manjari Sharma, Umesh Kumar, Shoorvir Singh

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Article
  2. Review
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  7. Multi-omics reveals a novel Cxcr4Clinical and translational medicine · 2026
    Article
  8. Review
  9. Article
  10. Article
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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

3 authors.

Manjari Sharma *Department of Biotechnology, GLA University, Mathura, Chaumuhan, Bharthia, 281406, Uttar Pradesh, India.
Umesh Kumar *University Institute of Engineering, Chandigarh University, NH-5, Chandigarh-Ludhiana Highway, Gharuan, Mohali, 140413, Punjab, India. umeshkumar82@gmail.com.
Shoorvir SinghDepartment of Biotechnology, GLA University, Mathura, Chaumuhan, Bharthia, 281406, Uttar Pradesh, India.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer is the leading cancer type that is reported in women worldwide, with its 2.3 million annual incidence and 685,000-related deaths (WHO, 2023). Although genetic mutations have proven to be major driving agents of tumorigenesis, the tumor microenvironment (TME) is increasingly being considered as the definitive indicator of disease progression, metastasis, immune evasion and therapeutic resistance. It is an active, diverse cellular webwork of substances cancer-related fibroblasts, (CAFs), tumor-related macrophages, (TAMs), regulatory T cells, (Tregs), myeloid-derived suppressor cells (MDSCs), and cancer-related adipocytes; (CAAs). These cellular processes interact reciprocally with not only malignant cells through paracrine communication but also through the composition of the extracellular matrix, (ECM). Recent research indicates that CAFs produce pro-invasive factors i.e. TGF-B and HGF whereas TAMs tend to be M2-like and secret VEGF and IL-10 to encourage angiogenesis and immune subversion. Cytokines, chemokines, ECM proteins, and tumor-derived EVs are non-cellular factors serving to alter cellular phenotypes and facilitate construction of metastatic niche. Besides oncogenic microRNAs (e.g., miR-21, miR-10b) that is released in exosome, hypoxia-mediated activation of HIF-1a induces both neovascularization and metabolic reprogramming. The repolarization of TAM (e.g. CSF1R inhibitors) and depletion of CAF and inhibition of EV pathway are also being explored as therapeutic mechanisms against TME resistance and are in preclinical and clinical development. In particular, the combination procedures with immunomodulation and TME disruption have demonstrated some success in conquering resistance in TNBC models. Therefore, it is paramount to understand how the surrounding tissue, the immune system, the immune system, and other elements behave over time and space as cofounding partners of tumors, in a way that would create better precision and clinical outcomes in breast cancer patients.

Indexed as

Breast NeoplasmsTumor MicroenvironmentAnimalsCancer-Associated FibroblastsCell CommunicationFemaleHumansMicroRNAsSignal TransductionMicroRNAsBreast cancerEpithelial- to- mesenchymal transition (EMT)Extracellular vesicles (EVs)MetastasisTargeted therapyTumor-associated macrophages (TAMs)Tumor microenvironment

Identifiers

What OpenQuestion holds

Textmetadata
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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 OpenQuestion graph.