ArticleClinical cancer research : an official journal of the American Association for Cancer Research2013
Modeling boundary conditions for balanced proliferation in metastatic latency.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Autophagy induced by metabolic processes leads to solid tumor cell metastatic dormancy and recurrence.Medical oncology (Northwood, London, England) · 2025Review
- Statins as Secondary Preventive Agent to Limit Breast Cancer Metastatic Outgrowth.International journal of molecular sciences · 2025Review
- Mesenchymal Stem Cell-Secreted Exosomes and Soluble Signals Regulate Breast Cancer Metastatic Dormancy: Current Progress and Future Outlook.International journal of molecular sciences · 2024Review
- Breast Cancer Metastatic Dormancy and Relapse: An Enigma of Microenvironment(s).Cancer research · 2022Review
- Microenvironment-mediated cancer dormancy: Insights from metastability theory.Proceedings of the National Academy of Sciences of the United States of America · 2022Review
- A Perspective on Therapeutic Pan-Resistance in Metastatic Cancer.International journal of molecular sciences · 2020Review
- Systems Biology of Cancer Metastasis.Cell systems · 2019Review
- Autophagy in breast cancer metastatic dormancy: Tumor suppressing or tumor promoting functions?Journal of cancer metastasis and treatment · 2019Article
- The great escape: How metastases of melanoma, and other carcinomas, avoid elimination.Experimental biology and medicine (Maywood, N.J.) · 2018Review
- Article
- Hydrogel microenvironments for cancer spheroid growth and drug screening.Science advances · 2018Review
- Inflammatory cytokine IL-8/CXCL8 promotes tumour escape from hepatocyte-induced dormancy.British journal of cancer · 2018Article
- EngineeredJournal of biological engineering · 2018Review
- Computational systems biology in cancer brain metastasis.Frontiers in bioscience (Scholar edition) · 2016Review
- Statin-induced mevalonate pathway inhibition attenuates the growth of mesenchymal-like cancer cells that lack functional E-cadherin mediated cell cohesion.Scientific reports · 2014Article
- Spontaneous dormancy of metastatic breast cancer cells in an all human liver microphysiologic system.British journal of cancer · 2014Article
- Mechanisms of disseminated cancer cell dormancy: an awakening field.Nature reviews. Cancer · 2014Review
- A microphysiological system model of therapy for liver micrometastases.Experimental biology and medicine (Maywood, N.J.) · 2014Review
- Hepatic nonparenchymal cells drive metastatic breast cancer outgrowth and partial epithelial to mesenchymal transition.Breast cancer research and treatment · 2014Article
- The dormancy dilemma: quiescence versus balanced proliferation.Cancer research · 2013Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
purposeNearly half of cancer metastases become clinically evident five or more years after primary tumor treatment; thus, metastatic cells survived without emerging for extended periods. This dormancy has been explained by at least two countervailing scenarios: cellular quiescence and balanced proliferation; these entail dichotomous mechanistic etiologies. To examine the boundary parameters for balanced proliferation, we conducted in silico modeling. EXPERIMENTAL
designTo illuminate the balanced proliferation hypothesis, we explored the specific boundary probabilities under which proliferating micrometastases would remain dormant. A two-state Markov chain Monte Carlo model simulated micrometastatic proliferation and death according to stochastic survival probabilities. We varied these probabilities across 100 simulated patients each with 1,000 metastatic deposits and documented whether the micrometastases exceeded one million cells, died out, or remained dormant (survived 1,218 generations).
resultsThe simulations revealed a narrow survival probability window (49.7-50.8%) that allowed for dormancy across a range of starting cell numbers, and even then for only a small fraction of micrometastases. The majority of micrometastases died out quickly even at survival probabilities that led to rapid emergence of a subset of micrometastases. Within dormant metastases, cell populations depended sensitively on small survival probability increments.
conclusionsMetastatic dormancy as explained solely by balanced proliferation is bounded by very tight survival probabilities. Considering the far larger survival variability thought to attend fluxing microenvironments, it is more probable that these micrometastatic nodules undergo at least periods of quiescence rather than exclusively being controlled by balanced proliferation.
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