ArticleFrontiers in oncology2018
Patterns of Tumor Progression Predict Small and Tissue-Specific Tumor-Originating Niches.
Article in Frontiers in oncology, 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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Who cites it
10 citing papers in PubMed.
- Cell competition driven by secreted ligands: Modeling liver metastasis of colorectal cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Cancer model with moving extinction threshold reproduces real cancer data.Journal of the Royal Society, Interface · 2025Article
- Biological Cargo: Exosomes and their Role in Cancer Progression and Metastasis.Current topics in medicinal chemistry · 2025Review
- Cancer-associated fibroblast related gene signature in Helicobacter pylori-based subtypes of gastric carcinoma for prognosis and tumor microenvironment estimationFrontiers in medicine · 2023Article
- Immunotoxicity of nanomaterials in health and disease: Current challenges and emerging approaches for identifying immune modifiers in susceptible populations.Wiley interdisciplinary reviews. Nanomedicine and nanobiotechnology · 2022Review
- New Advances in Biomedical Application of Polymeric Micelles.Pharmaceutics · 2022Review
- Modeling age-specific incidence of colon cancer via niche competition.PLoS computational biology · 2022Article
- Spatial structure governs the mode of tumour evolution.Nature ecology & evolution · 2022Article
- Time-extended exposure of gastric epithelial cells to secretome ofAmerican journal of cancer research · 2022Article
- Spondin 2 promotes the proliferation, migration and invasion of gastric cancer cells.Journal of cellular and molecular medicine · 2020Article
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The development of cancer is a multistep process in which cells increase in malignancy through progressive alterations. Such altered cells compete with wild-type cells and have to establish within a tissue in order to induce tumor formation. The range of this competition and the tumor-originating cell type which acquires the first alteration is unknown for most human tissues, mainly because the involved processes are hardly observable, aggravating an understanding of early tumor development. On the tissue scale, one observes different progression types, namely with and without detectable benign precursor stages. Human epidemiological data on the ratios of the two progression types exhibit large differences between cancers. The idea of this study is to utilize data of the ratios of progression types in human cancers to estimate the homeostatic range of competition in human tissues. This homeostatic competition range can be interpreted as necessary numbers of altered cells to induce tumor formation on the tissue scale. For this purpose, we develop a cell-based stochastic model which is calibrated with newly-interpreted human epidemiological data. We find that the number of tumor cells which inevitably leads to later tumor formation is surprisingly small compared to the overall tumor and largely depends on the human tissue type. This result points toward the existence of a tissue-specific tumor-originating niche in which the fate of tumor development is decided early and long before a tumor becomes detectable. Moreover, our results suggest that the fixation of tumor cells in the tumor-originating niche triggers new processes which accelerate tumor growth after normal tissue homeostasis is voided. Our estimate for the human colon agrees well with the size of the stem cell niche in colonic crypts. For other tissues, our results might aid to identify the tumor-originating cell type. For instance, data on primary and secondary glioblastoma suggest that the tumors originate from a cell type competing in a range of 300 - 1,900 cells.
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