Pancreatic cancer exosomes: left control, right exposed to Galahad
A Theoretical Novel Approach to Treating Cancer
Which came first, the virus or the cell? Logic says the cell because viruses can only replicate by entering cells and using the cell's replication machinery. But one can ask, if all viruses naturally have a key to open cell doors and use their replication machinery, then leave the cell damaged or destroyed, shouldn't the evolutionary process have changed cell door locks to block entry by a virus? But that hasn't happened. Why?
The only plausible explanation is that something resembling a virus is allowed by the cell to enter that same doorway because its presence is of great benefit to the cell's proper functioning. A reasonable theory of what that entity's benefit might cell communication an example being a role in helping control cell replication. It is known that cells need an external signal to initiate cellular replication. This could be a signal like a food source or a signal from another cell that has been primed by outside stimulation. In a multicellular organism, cell replication needs to be tightly controlled. Thus when growing a new part, it would be useful to maintain tight control of the growth process by using this entity's communication signals.
This concept is not so far-fetched when one considers that E. Pastuzyn et al(1) have shown that neurons produce non-replicating virus-like particles that are used for cellular communication. Since such structures are likely to have a degree of complexity, I term them "communications complexes." For eons they may have been the normal workers that have a key to the lock on the cell's door.
Hypothesis 1
It seems possible that all viruses originally morphed from a communication complex whose internal machinery became corrupted with an added replication algorithm coded into the information contained in its core. In essence, a virus may be a communications complex gone bad.
Since a virus is a non-living structure comprising an outer shell that targets specific cells and an inner core that provides information, one might hypothesize the structure that viruses mimic are these communications complexes that cells regularly use to help control their process of replicating. Such communication complexes do not have the ability to induce self-replication that is a hallmark of a virus.
Hypothesis 2
The human body has a broad spectrum of particles that have similar sizes and similar functions in maintaining the body's needs. It is known that growing cells need to receive signals from these particles or the cells will self-destruct. Exosomes are one of these particle types(2). A hypothesis is that if exosomes are signal carriers in the process of cancer cell growth(3), that growth can be halted if a non-toxic compound could be found that would inactivate those exosomes' signal-sending ability.
Experimental results
We have produced a new compound that is nontoxic and inactivates every virus it has been tested on (25 to date)(4) and every exosome (unpublished data, seven from cancer cell lines to date). This compound does not enter cells. Yet when we bathed cancer cell lines with this virus-inactivating and exosome-inactivating compound for more than one hour, the cancer cells died, no matter what part of the cell cycle they were in. However, if the compound was washed off before one hour, there was no effect on the cancer cell line.
In a human skin squamous cell cancer, we applied the compound once every 15 minutes for a 4-hour period. Over several months, this resulted in reducing the cancer size with normal skin regrowing in the areas where the cancer had died. This indicates there are three different mechanisms of cell growth:
1) Replacement growth such as when normal skin is replaced and is not governed by communication complex self-destruct feedback;
2) Repair that occurs when there is significant damage such as a cut that removes a chunk of skin and a scar results. (Again this is not governed by communication complex self-destruct feedback); and
3) Growth of a limb or organ which is critically controlled by communication complex self-destruct feedback. This is the mechanism of cancer.
Hypothesis 3—A novel new way to halt cancer's spread
A very promising line of cancer research will be to expose the virus-inactivating and exosome-inactivating compound noted above to a cancer line for a time long enough to stimulate cellular apoptosis by removal of the required cell communication and for the initiating cells to die. This is because all dangerous cancer is caused by the growth replication process initiated improperly by cell communication, and this compound has proven it can impact that cancerous process in a positive fashion.
Considerations in forming a treatment for cancer
The dose and timing of delivering the inactivating compound will depend on local blood flow and the amount of communication complexes produced by the initiating cells, and the treatment time will depend on the life of the initiating cells. Based on the NCI-60 panel of cell lines we had tested by Southern Research and the IC50 produced for each line, the range of the IC50s for all cancers were within a variant of plus or minus two times of the mean.
Conclusion
If this novel approach proves out, there should be no resistance by any cancers to this line of therapy.
Going forward
It is estimated that to fully treat a bulky high communication complex-producing cancer would require approximately two gallons of this newly discovered inactivating compound. This is based on an oral treatment of 100 ml ingested hourly for 10 hours in a row for several weeks. An ideal candidate to test would be someone with unresectable pancreatic cancer who can still ingest the fluid nutraceutical required.
We have a commercially produced nutraceutical grade source of this compound in both dry and liquid states, and a massive amount can be readily produced inexpensively.
References
1) Pastuzyn et al., 2018, Cell 172, 275–288 January 11, 2018 https://doi.org/10.1016/j.cell.2017.12.024
2) Guo et al., Oncology Reports 38: 665-675, 2017 https://doi.org/10.3892/or.2017.5714
3) Bastos et al., Seminars in Cell & Developmental Biology 78, 13-21 11 Aug 2017 https://doi.org/10.1016/j.semcdb2017.08.009
4) D.L. Barnard et al., Heliyon 8, e09887 1 July, 2022 https://doi.org/10.1016/j.heliyon.2022.e09887
