J Cancer 2015; 6(5):457-463. doi:10.7150/jca.10911 This issue Cite


Hypotheses of Cancer Weakening and Origin

John Cheung Yuen CHAN

33 Magnus St, Nelson Bay NSW 2315 Australia

CHAN JCY. Hypotheses of Cancer Weakening and Origin. J Cancer 2015; 6(5):457-463. doi:10.7150/jca.10911. https://www.jcancer.org/v06p0457.htm
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Approximately 2.7 billion years ago, cyanobacteria began producing oxygen by photosynthesis. Any free oxygen they produced was chemically captured by dissolved iron or organic matter. There was no ozone layer to protect living species against the radiation from space. Eukaryotic cells lived in water, under hypoxic environments, and metabolized glucose by fermentation. The Great Oxygenation Event (GOE) describes the point when oxygen sinks became saturated. This massive oxygenation of the Earth occurred approximately half a billion years ago. Species that evolved after the GOE are characterized by aerobic metabolism. Mammals evolved approximately a few hundred million years ago, with the ancient eukaryotic genes deeply embedded in their genome.

Many genes have been exchanged by horizontal gene transfer (HGT) throughout the history of cellular evolution. Mammals have been invaded by viruses, and while viral genetic relics are embedded in mammalian junk genes, not all junk genes are genetic relics of viruses. These viral relics have been inactivated through evolution and have little impact on mammalian life. However, there is evidence to suggest that these viral genetic relics are linked to cancer.

This hypothesis states that cancer develops when cell reproduction becomes defective because of the active involvement of viral genes, in a process similar to genetic engineering. Cancer cells are amalgamations of genetically modified organisms (GMOs). There are two main groups in cancer development. One group of cells arises by genetic engineering of a viral genetic relic, such as endogenous retroviruses (ERVs), which evolved after oxygenation of the atmosphere. This group is referred to here as genetically modified organisms from viral genes (GMOV). GMOVs may be inhibited by anticancer drugs. The second group arises by engineering of the genes of ancient eukaryotes, which existed prior to the oxygenation of the Earth. This second group is referred to as genetically modified organisms from ancient eukaryotic genes (GMOE). The GMOE group lives in hypoxic environments and metabolizes glucose by fermentation. GMOEs represent advanced cancer, which proliferate aggressively and are resistant to DNA damage.

It has been demonstrated that as an ERV becomes more prevalent in a mammalian genome, the possibility that the mammal will develop cancer increases. The hypothesis also states that most cancers have their origins in GMOV by the incorporation of viral genes from junk genes. As the cancer progresses, further subgroups of cancer GMOs will develop. If the cancer advances even further, the GMOE could eventually develop prior to late-stage cancer. Because the genes of ancient eukaryotes have enhanced innate immunity, GMOE will eventually prevail over the weaker GMOV during cancer subgroup competition. Hence, cancer development is mainly determined by genes in the mammalian genome.

An inherent weakness of cancer cells is their dependence on glucose and iron. Furthermore, they cannot tolerate physical disturbance. Ancient gene GMOs can be treated with a combination of mechanical vibration using glucose-coated magnetic nanoparticles and strengthening of the immune system. Herein, I suggest trials for verifying this hypothesis.

Keywords: Cancer origin, Viral genes, GMO, Nanoparticles

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CHAN, J.C.Y. (2015). Hypotheses of Cancer Weakening and Origin. Journal of Cancer, 6(5), 457-463. https://doi.org/10.7150/jca.10911.

CHAN, J.C.Y. Hypotheses of Cancer Weakening and Origin. J. Cancer 2015, 6 (5), 457-463. DOI: 10.7150/jca.10911.

CHAN JCY. Hypotheses of Cancer Weakening and Origin. J Cancer 2015; 6(5):457-463. doi:10.7150/jca.10911. https://www.jcancer.org/v06p0457.htm

CHAN JCY. 2015. Hypotheses of Cancer Weakening and Origin. J Cancer. 6(5):457-463.

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