ArticleBulletin of mathematical biology2018
Size Matters: Metastatic Cluster Size and Stromal Recruitment in the Establishment of Successful Prostate Cancer to Bone Metastases.
Article in Bulletin of mathematical biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 17 citations in OpenAlex.
- Overcoming vascular niche-mediated TKI resistance in acute myeloid leukemia through miR-126 inhibition.NPJ systems biology and applications · 2026Article
- Immune checkpoint inhibition in bone metastases: lesion response heterogeneity, the osteoimmune niche, and microenvironment-directed therapy.Frontiers in immunology · 2026Review
- Immunotherapy in the Battle Against Bone Metastases: Mechanisms and Emerging Treatments.Pharmaceuticals (Basel, Switzerland) · 2024Review
- 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
- How circulating tumor cluster biology contributes to the metastatic cascade: from invasion to dissemination and dormancy.Cancer metastasis reviews · 2023Review
- Intermetastatic and Intrametastatic Heterogeneity Shapes Adaptive Therapy Cycling Dynamics.Cancer research · 2023Article
- Classical mathematical models for prediction of response to chemotherapy and immunotherapy.PLoS computational biology · 2022Article
- An agent-based model of prostate Cancer bone metastasis progression and response to Radium223.BMC cancer · 2020Article
- Tumor Cell Dormancy and Reactivation in Bone: Skeletal Biology and Therapeutic Opportunities.JBMR plus · 2019Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Prostate cancer (PCa) impacts over 180,000 men every year in the USA alone, with 26,000 patients expected to succumb to the disease ( cancer.gov ). The primary cause of death is metastasis, with secondary lesions most commonly occurring in the skeleton. Prostate cancer to bone metastasis is an important, yet poorly understood, process that is difficult to explore with experimental techniques alone. To this end we have utilized a hybrid (discrete-continuum) cellular automaton model of normal bone matrix homeostasis that allowed us to investigate how metastatic PCa can disrupt the bone microenvironment. Our previously published results showed that PCa cells can recruit mesenchymal stem cells (MSCs) that give rise to bone-building osteoblasts. MSCs are also thought to be complicit in the establishment of successful bone metastases (Lu, in Mol Cancer Res 4(4):221-233, 2006). Here we have explored the aspects of early metastatic colonization and shown that the size of PCa clusters needs to be within a specific range to become successfully established: sufficiently large to maximize success, but not too large to risk failure through competition among cancer and stromal cells for scarce resources. Furthermore, we show that MSC recruitment can promote the establishment of a metastasis and compensate for relatively low numbers of PCa cells seeding the bone microenvironment. Combined, our results highlight the utility of biologically driven computational models that capture the complex and dynamic dialogue between cells during the initiation of active metastases.
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