ArticleScientific reports2016
A physical mechanism of cancer heterogeneity.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Unveiling the Dynamics behind Glioblastoma Multiforme Single-Cell Data Heterogeneity.International journal of molecular sciences · 2024Article
- Perspectives on the landscape and flux theory for describing emergent behaviors of the biological systems.Journal of biological physics · 2022Review
- Deciphering the molecular mechanism of the cancer formation by chromosome structural dynamics.PLoS computational biology · 2021Article
- Breast cancer: Muscarinic receptors as new targets for tumor therapy.World journal of clinical oncology · 2021Review
- Uncovering the Underlying Mechanisms of Cancer Metabolism through the Landscapes and Probability Flux Quantifications.iScience · 2020Article
- Multi-modality in gene regulatory networks with slow promoter kinetics.PLoS computational biology · 2019Article
- Mesenchymal stem cells over-expressing cxcl12 enhance the radioresistance of the small intestine.Cell death & disease · 2018Article
- Assessment of the toxicogenic effects and cell death potential of the ester (Z)-methyl 4-((1,5-dimethyl-3-oxo-2-phenyl-2,3-dihydro-1H-pyrazol-4-yl)amino)-4-oxobut-2-anoate in combination with cisplatin, cyclophosphamide and doxorubicin.Genetics and molecular biologyArticle
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We studied a core cancer gene regulatory network motif to uncover possible source of cancer heterogeneity from epigenetic sources. When the time scale of the protein regulation to the gene is faster compared to the protein synthesis and degradation (adiabatic regime), normal state, cancer state and an intermediate premalignant state emerge. Due to the epigenetics such as DNA methylation and histone remodification, the time scale of the protein regulation to the gene can be slower or comparable to the protein synthesis and degradation (non-adiabatic regime). In this case, many more states emerge as possible phenotype alternations. This gives the origin of the heterogeneity. The cancer heterogeneity is reflected from the emergence of more phenotypic states, larger protein concentration fluctuations, wider kinetic distributions and multiplicity of kinetic paths from normal to cancer state, higher energy cost per gene switching, and weaker stability.
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