ReviewFrontiers in immunology2015
Hyaluronan, Inflammation, and Breast Cancer Progression.
Review in Frontiers in immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 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
109 citing papers in PubMed, 187 citations in OpenAlex.
- Epigenetic Silencing of CYYR1 Promotes Lung Adenocarcinoma Progression Through TRIM21-Dependent Regulation of HMMR Stability.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Proteoglycans as Molecular Regulators of Bone Metastasis: Extracellular Matrix Remodeling, Tumor-Bone Crosstalk, Dormancy, and Therapeutic Opportunities.Biomolecules · 2026Review
- Extracellular matrix mediates circulating tumor cell clustering in triple-negative breast cancer metastasis.Nature communications · 2026Article
- Dysregulated hyaluronan metabolism drives inflammation and angiogenesis in proliferative diabetic retinopathy.Frontiers in immunology · 2026Article
- Article
- Glycosaminoglycans Targeted by Colchicine in MCF-7 Cells.Pharmaceutics · 2025Article
- Integrated bioinformatics analysis of common molecular mechanisms and biomarkers in oral squamous cell carcinoma and periodontal disease.Discover oncology · 2025Article
- Oncotransformation in Bhas 42 Cell Transformation Assay by Typical Non-Genotoxic Carcinogens, PFOA and PFOS, and Time-Course Transcriptome Analysis.Biomolecules · 2025Article
- Matrix: a complex amalgam of structures and functions in tumor microenvironment.FEBS open bio · 2025Review
- Receptor for Hyaluronan Mediated Motility (RHAMM)/Hyaluronan Axis in Breast Cancer Chemoresistance.Cancers · 2024Article
- Breast Cancer: Extracellular Matrix and Microbiome Interactions.International journal of molecular sciences · 2024Review
- Nomogram for preoperative differentiation of benign and malignant breast tumors using contrast-enhanced cone-beam breast CT (CE CB-BCT) quantitative imaging and assessment features.La Radiologia medica · 2024Article
- Functional delineation of the luminal epithelial microenvironment in breast using cell-based screening in combinatorial microenvironments.Cellular signalling · 2024Article
- Reaching the Tumor: Mobility of Polymeric Micelles Inside anACS applied materials & interfaces · 2023Article
- 3D bioprinted breast tumor-stroma models for pre-clinical drug testing.Materials today. Bio · 2023Article
- Change in gliding properties of the iliotibial tract in hypermobile Ehlers-Danlos Syndrome.Journal of ultrasound · 2023Article
- The Hyaluronan/CD44 Axis: A Double-Edged Sword in Cancer.International journal of molecular sciences · 2023Review
- Targeting CD44 Receptor Pathways in Degenerative Joint Diseases: Involvement of Proteoglycan-4 (PRG4).Pharmaceuticals (Basel, Switzerland) · 2023Review
- CD44 Modulates Cell Migration and Invasion in Ewing Sarcoma Cells.International journal of molecular sciences · 2023Article
- Receptor for hyaluronan-mediated motility (RHAMM) defines an invasive niche associated with tumor progression and predicts poor outcomes in breast cancer patients.The Journal of pathology · 2023Article
49 more citing papers are in PubMed but not listed here.
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 at 4 institutions in 2 countries.
Funding
Abstract
Breast cancer-induced inflammation in the tumor reactive stroma supports invasion and malignant progression and is contributed to by a variety of host cells including macrophages and fibroblasts. Inflammation appears to be initiated by tumor cells and surrounding host fibroblasts that secrete pro-inflammatory cytokines and chemokines and remodel the extracellular matrix (ECM) to create a pro-inflammatory "cancerized" or tumor reactive microenvironment that supports tumor expansion and invasion. The tissue polysaccharide hyaluronan (HA) is an example of an ECM component within the cancerized microenvironment that promotes breast cancer progression. Like many ECM molecules, the function of native high-molecular weight HA is altered by fragmentation, which is promoted by oxygen/nitrogen free radicals and release of hyaluronidases within the tumor microenvironment. HA fragments are pro-inflammatory and activate signaling pathways that promote survival, migration, and invasion within both tumor and host cells through binding to HA receptors such as CD44 and RHAMM/HMMR. In breast cancer, elevated HA in the peri-tumor stroma and increased HA receptor expression are prognostic for poor outcome and are associated with disease recurrence. This review addresses the critical issues regarding tumor-induced inflammation and its role in breast cancer progression focusing specifically on the changes in HA metabolism within tumor reactive stroma as a key factor in malignant progression.
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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 OpenQuestion graph.