ArticleAging2014
Stochastic modeling indicates that aging and somatic evolution in the hematopoetic system are driven by non-cell-autonomous processes.
Article in Aging, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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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
36 citing papers in PubMed.
- Review
- A Poisson distribution-based general model of cancer rates and a cancer risk-dependent theory of aging.Aging · 2023Article
- Aging microenvironment and antitumor immunity for geriatric oncology: the landscape and future implications.Journal of hematology & oncology · 2023Review
- Mesenchymal stromal cell senescence in haematological malignancies.Cancer metastasis reviews · 2023Review
- Inflammation as a regulator of hematopoietic stem cell function in disease, aging, and clonal selection.The Journal of experimental medicine · 2021Review
- The Dynamic Interface Between the Bone Marrow Vascular Niche and Hematopoietic Stem Cells in Myeloid Malignancy.Frontiers in cell and developmental biology · 2021Review
- Normal Aging and Its Role in Cancer Metastasis.Cold Spring Harbor perspectives in medicine · 2020Review
- How the ageing microenvironment influences tumour progression.Nature reviews. Cancer · 2020Review
- Interplay Between Diabetes and Pancreatic Ductal Adenocarcinoma and Insulinoma: The Role of Aging, Genetic Factors, and Obesity.Frontiers in endocrinology · 2020Review
- A mathematical solution to Peto's paradox using Polya's urn model: implications for the aetiology of cancer in general.Theory in biosciences = Theorie in den Biowissenschaften · 2019Article
- Decoy fitness peaks, tumor suppression, and aging.Aging cell · 2019Article
- Article
- Aged marrow macrophages expand platelet-biased hematopoietic stem cells via Interleukin1B.JCI insight · 2019Article
- Chromosome integrity checkpoints in stem and progenitor cells: transitions upon differentiation, pathogenesis, and aging.Cellular and molecular life sciences : CMLS · 2018Review
- Up-Regulation of PI 3-Kinases and the Activation of PI3K-Akt Signaling Pathway in Cancer Stem-Like Cells Through DNA Hypomethylation Mediated by the Cancer Microenvironment.Translational oncology · 2018Article
- The relationship of mammal survivorship and body mass modeled by metabolic and vitality theories.Population ecology · 2018Article
- Connecting Cancer to Its Causes Requires Incorporation of Effects on Tissue Microenvironments.Cancer research · 2017Article
- MicroRNAs and the metabolic hallmarks of aging.Molecular and cellular endocrinology · 2017Review
- Aging, Metabolism, and Cancer Development: from Peto's Paradox to the Warburg Effect.Aging and disease · 2017Review
- Non-cell-autonomous effects yield lower clonal diversity in expanding tumors.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Age-dependent tissue decline and increased cancer incidence are widely accepted to be rate-limited by the accumulation of somatic mutations over time. Current models of carcinogenesis are dominated by the assumption that oncogenic mutations have defined advantageous fitness effects on recipient stem and progenitor cells, promoting and rate-limiting somatic evolution. However, this assumption is markedly discrepant with evolutionary theory, whereby fitness is a dynamic property of a phenotype imposed upon and widely modulated by environment. We computationally modeled dynamic microenvironment-dependent fitness alterations in hematopoietic stem cells (HSC) within the Sprengel-Liebig system known to govern evolution at the population level. Our model for the first time integrates real data on age-dependent dynamics of HSC division rates, pool size, and accumulation of genetic changes and demonstrates that somatic evolution is not rate-limited by the occurrence of mutations, but instead results from aged microenvironment-driven alterations in the selective/fitness value of previously accumulated genetic changes. Our results are also consistent with evolutionary models of aging and thus oppose both somatic mutation-centric paradigms of carcinogenesis and tissue functional decline. In total, we demonstrate that aging directly promotes HSC fitness decline and somatic evolution via non-cell-autonomous mechanisms.
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