ArticleBoneKEy reports2012
The role of TGF-β in bone metastasis: novel therapeutic perspectives.
Article in BoneKEy reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 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
60 citing papers in PubMed, 93 citations in OpenAlex.
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- From Bone Marrow Reserve to Metastatic Niche: How Neutrophil-Lineage Cells Shape Skeletal Colonization.International journal of molecular sciences · 2026Review
- Research Progress on Signaling Pathways in Breast Cancer Bone Metastasis.Oncology research · 2026Review
- The immune landscape of systemic inflammation in prostate cancer.Cancer biology & medicine · 2025Review
- Bridging the Gap in Understanding Bone Metastasis: A Multifaceted Perspective.International journal of molecular sciences · 2024Review
- A Novel Primary Cilium-Mediated Mechanism Through which Osteocytes Regulate Metastatic Behavior of Both Breast and Prostate Cancer Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Impact of cell plasticity on prostate tumor heterogeneity and therapeutic response.American journal of clinical and experimental urology · 2024Review
- Calcium signalling pathways in prostate cancer initiation and progression.Nature reviews. Urology · 2023Review
- Beyond boundaries: unraveling innovative approaches to combat bone-metastatic cancers.Frontiers in endocrinology · 2023Review
- EZH2 engages TGFβ signaling to promote breast cancer bone metastasis via integrin β1-FAK activation.Nature communications · 2022Article
- Review
- The gut microbiota can be a potential regulator and treatment target of bone metastasis.Biochemical pharmacology · 2022Review
- The Osteoclast Traces the Route to Bone Tumors and Metastases.Frontiers in cell and developmental biology · 2022Review
- Correlation between Tumor Microenvironment and Immune Subtypes Based on CD8 T Cells Enhancing Personalized Therapy of Gastric Cancer.Journal of oncology · 2022Article
- Suppression of breast cancer-associated bone loss with osteoblast proteomes via Hsp90ab1/moesin-mediated inhibition of TGFβ/FN1/CD44 signaling.Theranostics · 2022Article
- The Role of TGF-β in Bone Metastases.Biomolecules · 2021Review
- Review
- A Role for TGFβ Signaling in Preclinical Osteolytic Estrogen Receptor-Positive Breast Cancer Bone Metastases Progression.International journal of molecular sciences · 2021Article
- Acetylation of KLF5 maintains EMT and tumorigenicity to cause chemoresistant bone metastasis in prostate cancer.Nature communications · 2021Article
- Immune Checkpoint Inhibitor Therapy for Bone Metastases: Specific Microenvironment and Current Situation.Journal of immunology research · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
The skeleton is a preferred site for cancer metastasis. These bone metastases cause dysregulated bone remodeling and the associated morbidity of fractures, pain, hypercalcemia and catastrophic nerve compression syndromes. Transforming growth factor-β (TGF-β) is stored in mineralized bone matrix, and released and activated by osteoclastic bone resorption. Once activated, TGF-β stimulates nearby metastatic tumor cells within the bone microenvironment to secrete factors that further drive osteolytic destruction of the bone. Therefore, TGF-β and its signaling constitute a critical component driving the feed-forward vicious cycle of cancer growth in bone. Moreover, additional pro-tumorigenic activities attributed to TGF-β include activation of epithelial-to-mesenchymal transition, increased tumor cell invasion, enhanced angiogenesis and various immunomodulatory properties. Blocking the TGF-β signaling pathway to interrupt this vicious cycle and manipulate the bone microenvironment offers a promising area for therapeutic intervention to decrease skeletal metastasis and normalize bone homeostatic mechanisms. In this review, preclinical and clinical data are evaluated for the potential use of TGF-β pathway inhibitors in clinical practice to treat bone metastases and its associated comorbidities.
Identifiers
What 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.