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Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate (DMBA-TPA)
Published on: December 19, 2019
Models of carcinogenesis: an overview.
Paolo Vineis1, Arthur Schatzkin, John D Potter
1Department of Epidemiology and Public Health, MRC/HPA Centre for Environment and Health, School of Public Health, Imperial College London, Norfolk Place, London W2 1PG, UK. p.vineis@imperial.ac.uk
Carcinogenesis
|May 1, 2010
Summary
Cancer research has seen five models of carcinogenesis, including mutation, genome instability, and epigenetics. A new model integrates these, proposing two main types based on epithelial or stromal changes for malignancy.
Area of Science:
- Oncology
- Cancer Research
- Cell Biology
Background:
- Over the last century, multiple models of carcinogenesis have been developed.
- These models focus on genetic mutations, genome instability, non-genotoxic mechanisms, and tissue organization.
Purpose of the Study:
- To review and categorize existing models of carcinogenesis.
- To propose a unifying framework for understanding cancer development.
- To provide a basis for formulating new research hypotheses.
Main Methods:
- Review of historical and current carcinogenesis models.
- Mathematical formalization of five distinct models.
- Categorization of models into two overarching types.
Main Results:
- Five main models of carcinogenesis are described: mutation-centric, genome instability, non-genotoxic mechanisms, somatic cellular selection, and tissue organization.
- These models largely overlap but are presented separately for clarity.
- A simplified scheme of two model types is proposed: epithelial changes alone, or combined epithelial and stromal changes.
Conclusions:
- The proposed framework integrates previous models of carcinogenesis.
- This simplified scheme captures the historical progression of cancer theories.
- The framework can aid in making cancer research hypotheses more explicit.
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