ArticleCancer research2014
An integrated computational model of the bone microenvironment in bone-metastatic prostate cancer.
Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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.
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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.
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Who cites it
57 citing papers in PubMed, 100 citations in OpenAlex.
- Next-generation osteosarcoma models for precision medicine.Communications biology · 2026Review
- Decoding the Role of MDSCs in Bone Metastasis: Multicellular Interactions and Clinical Implications.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Overcoming vascular niche-mediated TKI resistance in acute myeloid leukemia through miR-126 inhibition.NPJ systems biology and applications · 2026Article
- 75 Years of Mathematical Oncology.bioRxiv : the preprint server for biology · 2026Article
- Targeted Deletion of Cxcl1 in MSCs Regulates Osteogenesis and Suppresses Bone-Metastatic Prostate Cancer.Molecular cancer research : MCR · 2025Article
- Exploring bone-tumor interactions through 3DJournal of bone oncology · 2025Review
- Blood-based detection of MMP11 as a marker of prostate cancer progression regulated by the ALDH1A1-TGF-β1 signaling mechanism.Journal of experimental & clinical cancer research : CR · 2025Article
- Mechanobiological cues to bone cells during early metastasis drive later osteolysis: A computational mechanoregulation framework prediction.Mechanobiology in medicine · 2025Article
- Computational simulations of endocrine bone diseases related to pathological glandular PTH secretion using a multi-scale bone cell population model.Frontiers in bioengineering and biotechnology · 2025Article
- A Multicellular Mechanochemical Model to Investigate Tumor Microenvironment Remodeling and Pre-Metastatic Niche Formation.Cellular and molecular bioengineering · 2024Article
- Dissecting the Spatially Restricted Effects of Microenvironment-Mediated Resistance on Targeted Therapy Responses.Cancers · 2024Article
- A seven-step guide to spatial, agent-based modelling of tumour evolution.Evolutionary applications · 2024Review
- The bone ecosystem facilitates multiple myeloma relapse and the evolution of heterogeneous drug resistant disease.Nature communications · 2024Article
- A review of mathematical modeling of bone remodeling from a systems biology perspective.Frontiers in systems biology · 2024Article
- Synthetic living materials in cancer biology.Nature reviews bioengineering · 2023Article
- Androgen receptor inhibition suppresses anti-tumor neutrophil response against bone metastatic prostate cancer via regulation of TβRI expression.Cancer letters · 2023Article
- Mutation divergence over space in tumour expansion.Journal of the Royal Society, Interface · 2023Article
- Review
- Agent-based methods facilitate integrative science in cancer.Trends in cell biology · 2023Review
- An agent-based model of cardiac allograft vasculopathy: toward a better understanding of chronic rejection dynamics.Frontiers in bioengineering and biotechnology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Bone metastasis will impact most men with advanced prostate cancer. The vicious cycle of bone degradation and formation driven by metastatic prostate cells in bone yields factors that drive cancer growth. Mechanistic insights into this vicious cycle have suggested new therapeutic opportunities, but complex temporal and cellular interactions in the bone microenvironment make drug development challenging. We have integrated biologic and computational approaches to generate a hybrid cellular automata model of normal bone matrix homeostasis and the prostate cancer-bone microenvironment. The model accurately reproduces the basic multicellular unit bone coupling process, such that introduction of a single prostate cancer cell yields a vicious cycle similar in cellular composition and pathophysiology to models of prostate-to-bone metastasis. Notably, the model revealed distinct phases of osteolytic and osteogenic activity, a critical role for mesenchymal stromal cells in osteogenesis, and temporal changes in cellular composition. To evaluate the robustness of the model, we assessed the effect of established bisphosphonate and anti-RANKL therapies on bone metastases. At approximately 100% efficacy, bisphosphonates inhibited cancer progression while, in contrast with clinical observations in humans, anti-RANKL therapy fully eradicated metastases. Reducing anti-RANKL yielded clinically similar results, suggesting that better targeting or dosing could improve patient survival. Our work establishes a computational model that can be tailored for rapid assessment of experimental therapies and delivery of precision medicine to patients with prostate cancer with bone metastases.
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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.