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Cancer as a mechanism of hypermutation
1U.S. Army Ballistic Research Laboratory, Aberdeen Proving Ground, MD 21005.
Acta Biotheoretica
|March 1, 1992
Summary
Cancer may be a phylogenetic mechanism for "hyperevolution," not just a dysfunction. This process, observed in bacterial mutations, utilizes cell mechanisms for evolutionary advantage, even at the expense of individual development.
Area of Science:
- Oncology
- Evolutionary Biology
- Genetics
Background:
- Cancers exhibit structured mechanisms and respond to environmental stress.
- The existence of oncogenes suggests neoplasticity may have a biological function beyond dysfunction.
- Recent discoveries in bacterial mutations reveal a similar process of
- hyperevolution
- .
Purpose of the Study:
- To propose that cancer functions as a phylogenetic mechanism for hyperevolution.
- To explore the mechanisms underlying cancer-mediated hyperevolution.
- To analyze the evolutionary advantage conferred by stress-induced neoplasticity.
Main Methods:
- Analysis of cancer's structured mechanisms and response to environmental stress.
- Investigation of cell-surface-associated nucleic acid in tumorigenic cells.
- Examination of sperm cell vectorization of foreign DNA.
Main Results:
- Neoplasticity may serve as a phylogenetic mechanism for hyperevolution, similar to bacterial mutation processes.
- Cell-surface nucleic acid and sperm cell DNA vectorization are key mechanisms for cancer-mediated hyperevolution.
- Stress-induced neoplasticity provides an evolutionary advantage exceeding two orders of magnitude for chemical cytology mutagenesis.
Conclusions:
- Cancer represents a hyperevolutionary phylogenetic mechanism, not merely a biological dysfunction.
- Essential mechanisms involving cell-surface nucleic acid and sperm cell vectorization facilitate cancer-mediated hyperevolution.
- Stress-induced neoplasticity offers a significant evolutionary advantage in mutagenesis.
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