ReviewProgress in biophysics and molecular biology2016
Carcinogenesis explained within the context of a theory of organisms.
Review in Progress in biophysics and molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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
45 citing papers in PubMed.
- The Future of Breast Cancer Treatment: From Conventional Wisdom to Nanotechnology-Enabled Precision.International journal of molecular sciences · 2026Review
- Bioelectricity is a universal multifaced signaling cue in living organisms.Molecular biology of the cell · 2025Review
- The systemic evolutionary theory of the origin of cancer (SETOC): an update.Molecular medicine (Cambridge, Mass.) · 2025Article
- Ferroptosis contributes to the progression of female-specific neoplasms, from breast cancer to gynecological malignancies in a manner regulated by non-coding RNAs: Mechanistic implications.Non-coding RNA research · 2024Review
- The theragnostic advances of exosomes in managing leukaemia.Journal of cellular and molecular medicine · 2024Review
- Article
- Is Cancer Metabolism an Atavism?Cancers · 2024Review
- Initiation of Cancer: The Journey From Mutations in Somatic Cells to Epigenetic Changes in Tissue-resident VSELs.Stem cell reviews and reports · 2024Review
- Bioinformatic analysis reveals an association between Metadherin with breast cancer prognosis and tumor immune infiltration.Scientific reports · 2024Article
- Modeling Mammary Organogenesis from Biological First Principles: A Systems Biology Approach.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Bio-Hacking Better Health-Leveraging Metabolic Biochemistry to Maximise Healthspan.Antioxidants (Basel, Switzerland) · 2023Article
- Autophagy modulators influence the content of important signalling molecules in PS-positive extracellular vesicles.Cell communication and signaling : CCS · 2023Article
- Adopted neoplastic cells and the consequences of their existence.Oncotarget · 2023Article
- Conditional expression of endorepellin in the tumor vasculature attenuates breast cancer growth, angiogenesis and hyaluronan deposition.Matrix biology : journal of the International Society for Matrix Biology · 2023Article
- FN1 overexpression is correlated with unfavorable prognosis and immune infiltrates in breast cancer.Frontiers in genetics · 2022Article
- Mutation or not, what directly establishes a neoplastic state, namely cellular immortality and autonomy, still remains unknown and should be prioritized in our research.Journal of Cancer · 2022Review
- Generation of a uniform thymic malignant lymphoma model with C57BL/6JJournal of toxicologic pathology · 2022Article
- Review
- The cancer puzzle: Welcome to organicism.Progress in biophysics and molecular biology · 2021Article
- From Wingspread to CLARITY: a personal trajectory.Nature reviews. Endocrinology · 2021Review
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
For a century, the somatic mutation theory (SMT) has been the prevalent theory to explain carcinogenesis. According to the SMT, cancer is a cellular problem, and thus, the level of organization where it should be studied is the cellular level. Additionally, the SMT proposes that cancer is a problem of the control of cell proliferation and assumes that proliferative quiescence is the default state of cells in metazoa. In 1999, a competing theory, the tissue organization field theory (TOFT), was proposed. In contraposition to the SMT, the TOFT posits that cancer is a tissue-based disease whereby carcinogens (directly) and mutations in the germ-line (indirectly) alter the normal interactions between the diverse components of an organ, such as the stroma and its adjacent epithelium. The TOFT explicitly acknowledges that the default state of all cells is proliferation with variation and motility. When taking into consideration the principle of organization, we posit that carcinogenesis can be explained as a relational problem whereby release of the constraints created by cell interactions and the physical forces generated by cellular agency lead cells within a tissue to regain their default state of proliferation with variation and motility. Within this perspective, what matters both in morphogenesis and carcinogenesis is not only molecules, but also biophysical forces generated by cells and tissues. Herein, we describe how the principles for a theory of organisms apply to the TOFT and thus to the study of carcinogenesis.
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