ReviewInternational journal of molecular sciences2019
The Systemic-Evolutionary Theory of the Origin of Cancer (SETOC): A New Interpretative Model of Cancer as a Complex Biological System.
Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Tracing Genetic Images Formed During Evolution.International journal of molecular sciences · 2026Article
- The systemic evolutionary theory of the origin of cancer (SETOC): an update.Molecular medicine (Cambridge, Mass.) · 2025Article
- The Spiral Model of Evolution: Stable Life Forms of Organisms and Unstable Life Forms of Cancers.International journal of molecular sciences · 2024Review
- Is Cancer Metabolism an Atavism?Cancers · 2024Review
- Realizing the promise of Project Optimus: Challenges and emerging opportunities for dose optimization in oncology drug development.CPT: pharmacometrics & systems pharmacology · 2024Review
- Integrating frontiers: a holistic, quantum and evolutionary approach to conquering cancer through systems biology and multidisciplinary synergy.Frontiers in oncology · 2024Review
- Clinical Tumor Dormancy.Methods in molecular biology (Clifton, N.J.) · 2024Review
- Exploring the Therapeutic Potential of Ethyl 3-Hydroxybutyrate in Alleviating Skeletal Muscle Wasting in Cancer Cachexia.Biomolecules · 2023Article
- Cellular Adaptation Takes Advantage of Atavistic Regression Programs during Carcinogenesis.Cancers · 2023Review
- Cellular and Genetic Background of Osteosarcoma.Current issues in molecular biology · 2023Review
- DNA Damage Response-Related Proteins Are Prognostic for Outcome in Both Adult and Pediatric Acute Myelogenous Leukemia Patients: Samples from Adults and from Children Enrolled in a Children's Oncology Group Study.International journal of molecular sciences · 2023Article
- What Are the Reasons for Continuing Failures in Cancer Therapy? Are Misleading/Inappropriate Preclinical Assays to Be Blamed? Might Some Modern Therapies Cause More Harm than Benefit?International journal of molecular sciences · 2022Review
- Life Entrapped in a Network of Atavistic Attractors: How to Find a Rescue.International journal of molecular sciences · 2022Review
- 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
- Metabolic therapy and bioenergetic analysis: The missing piece of the puzzle.Molecular metabolism · 2021Review
- A Significant Question in Cancer Risk and Therapy: Are Antibiotics Positive or Negative Effectors? Current Answers and Possible Alternatives.Antibiotics (Basel, Switzerland) · 2020Review
- The perplexity of targeting genetic alterations in hepatocellular carcinoma.Medical oncology (Northwood, London, England) · 2020Article
- Intratumor Heterogeneity and Therapy Resistance: Contributions of Dormancy, Apoptosis Reversal (Anastasis) and Cell Fusion to Disease Recurrence.International journal of molecular sciences · 2020Review
- The Promising Connection Between Data Science and Evolutionary Theory in Oncology.Frontiers in oncology · 2019Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Systemic-Evolutionary Theory of Cancer (SETOC) is a recently proposed theory based on two important concepts: (i) Evolution, understood as a process of cooperation and symbiosis (Margulian-like), and (ii) The system, in terms of the integration of the various cellular components, so that the whole is greater than the sum of the parts, as in any complex system. The SETOC posits that cancer is generated by the de-emergence of the "eukaryotic cell system" and by the re-emergence of cellular subsystems such as archaea-like (genetic information) and/or prokaryotic-like (mitochondria) subsystems, featuring uncoordinated behaviors. One of the consequences is a sort of "cellular regression" towards ancestral or atavistic biological functions or behaviors similar to those of protists or unicellular organisms in general. This de-emergence is caused by the progressive breakdown of the endosymbiotic cellular subsystem integration (mainly, information = nucleus and energy = mitochondria) as a consequence of long-term injuries. Known cancer-promoting factors, including inflammation, chronic fibrosis, and chronic degenerative processes, cause prolonged damage that leads to the breakdown or failure of this form of integration/endosymbiosis. In normal cells, the cellular "subsystems" must be fully integrated in order to maintain the differentiated state, and this integration is ensured by a constant energy intake. In contrast, when organ or tissue damage occurs, the constant energy intake declines, leading, over time, to energy shortage, failure of endosymbiosis, and the de-differentiated state observed in dysplasia and cancer.
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Registered trials
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