Cancer Theory

This blog will elucidate the mechanism of cancer and show why only a full understanding of genomic reactions can result in complete and definitive cures. I developed this theory about 20 years ago. I now publish it because in that time I haven’t seen anything quite the same and I hope that it might encourage someone to test the idea experimentally.  Twenty years ago I heard of a woman biologist who placed cancer cells in an embryo and found that the cancer cells went back to normal. This theory is an attempt to explain that finding. I call it the Cell Recognition Theory. All comments and questions would be welcome.  One billion years ago there was a unicellular organism that underwent a mitotic division but rather than separate completely, the two cells decided to stick together and call themselves multi-cellular. This held some advantage. Perhaps it did nothing more than create a heavier organism that remained sessile thereby saving energy by allowing food to come to it. To e...

Joshua Chu and others have shown that microgravity hinders the cancer cell. This is not surprising being that a cell needs to anchor itself before it can pull apart its chromosomes. Unable to pull apart the chromosomes, a cancer cell would then stop dividing or, thanks to numerous checkpoints, would not even start the process. I still haven't determined definitively whether the CRF's are the molecules anchoring the cell. I don't think they are because prior to multicellularity, animal cells still needed to anchor themselves prior to cell division and would have cell surface molecules specifically for that purpose. I don't know of any free-swimming unicellular animals that do not require anchoring in order to reproduce. The free-swimming yeast cell has a rigid cellulose wall with which to anchor its microtubules.

[ note: contains adult discussions of sexual matters which some non-biologists may find offensive ] St. Peregrinus is the patron saint of those suffering from cancer but his connection to this blog goes deeper than that, and it's something that I've been meaning to write about. if the CRF Theory demands a loss of communication between cells as the initiator of cancer, what role would physical factors play? I've refrained from discussing this because the evidence is very anecdotal. But let's start with the saint. In penance for his actions, he spent 30 years preferring standing to sitting, and he ended up with varicosities of the leg and, eventually, cancer of the foot which was so bad that an amputation was scheduled* The caveat that makes cancer etiology so difficult is that rarely does a single factor produce cancer for even when a single factor has a causal relationship, there are some who do not succumb to it. Multiple factors enter into the equation--the patien...

Cancer that runs in families may be evolution in action. When an evolutionary change takes place, other cells may have to undergo simultaneous change. This is because no cell other than free-floating blood cells can remain unattached to at least one other cell. Blodd cells can do it because they are fully diffentiated as free-floating. Other cells need to know where they are and they do it by a kind of "hand-shaking" or lock/key mechanism (ie, what I have been calling Cell Recognition Factors. If we accept the fact that cells need to communicate with their neighbors, we can see that evolutionary changes involving changes in stucture will result in cancer until such time that neighboring cells can provide the right signals. This explains why evolution is such a slow process no cell undergoing a change can completel it's change without another cell matching its CRF.

http://www.technologyreview.com/Biotech/19039/ Technology is quickly gathering tools to help in characterizing the cell surface antigens or the RF's (recognition factors) that play a central role in cancer. We will create molecules that will "label" a cancer cell as producing certain CSA/RF's. Once we know where the cancer cell is in terms of it's present programming (remember, the existing CSA/RF is indicative of the particular cancer "stage"), we can present the cell with embryonic RF's that may alter the cell's behavior.

NewsFox (174) A group of researchers have converted fibroblasts (connective tissue cells) to cells which greatly resemble embryonic cells. They looked at the histone structure and it is nearly the same as that found in embryonic cells. That is, the DNA was programmed to an early stage. No mention was made of the use of such cells in Cancer but, if my theory is correct, injecting such cells into cancerous growths could revert the cancer to normal cells. It remains to be seen if the cancer will revert to what it was before turning cancerous or if the cancer will differentiate into an embryo-like structure. If the latter, then we still have to deal with a "growth" but it probably will have lost its malignant properties. It should not continue to differentiate into a fetus because a fetus needs a womb to continue its development. It may be that no surgical intervention will be required because the body's own defenses (lymphocytes) may have time to attack the cancer. The immun...

I'm still waiting for the magic moment that will tell me that biologists are using cell surface antigens to reprogram cancer cells. However, there was news recently about how scientists are closely examining histones as a means towards reprogramming. You see, histones are used by the cell to keep DNA in check. As any of you who have had the misfortune of having to unravel a ball of string know, stringy material like DNA would be impossible to keep orderly if there weren't some means of keeping them neatly spooled. This is where histones come in. They are the spools for DNA. It seems as if there might be a mechanism in place-involving histones--whereby the histones are manipulated by epigenetic factors in order to facilitate or defacilitate the transcription of DNA. In other words, Cancer cells are causing certain histones to allow a certain DNA expression. If we can shut down the active histones, we may be able to shut down cancer; but this would only work if histones were foun...

I heard this recently but because I'm so busy with other stuff, I can't reference it. It seems that cells of the embryo can migrate into the mother's brain and differentiate there into maternal brain cells. This shows that embryonic cells when separated from source tissue can continue their differentiation elsewhere--even in tissue from a different individual. It is able to do this because embryonic and maternal RF's were the same. If this effect was demonstrated in non-inbred individuals then it shows that RF expression is a random process and, occasionally, the maternal and embryonic RF's are the same.

news @ nature.com�-�Human stem cells trigger immune attack�-�Doubt cast on therapeutic use of embryonic cell lines. If my theory of Cell Recognition Factors is correct, this immune attack is happening for reasons besides the assimilation of foreign molecules into lab-grown cells. Remember that an embryonic cell when growing in utero expresses a different set of RF's. This enables the placenta to wall it off from maternal attack. If it had RF's the same as that of the mother, the embryo would invade the maternal tissues just like a cancer does. A prediction of this theory is that stem cell implantation would not work unless matched for RF's. Now, as humans, we all have the same set of RF's but only a subset is expressed. The question that needs to be answered is this: what is the basis for selecting one subset over another? Is it random or is it selected based on RF's already present in the embryonic cell's early environment. Either way, the developing emb...

Theory to Practice. This article shows one avenue of attack using R-factors. This company has come up with a means of 'ungluing" cancer cells. We know from previous blog entries that when a cell becomes unglued or otherwise loses communication with its neighbours, it has two courses of action available: cell suicide (apoptosis) or recycling to an earlier stage of development. Cancer cells are already at a very early stage of development and hence may opt for apoptosis instead; this is what the biotech company is counting on--I think this is very promising. The 'glues' spoken of in this article are a class of compounds called cadherins and I don't know at this point whether they are the R-factors that this blog talks about or whether they are a more generic substance that holds cells together after R-factors have established communicaiton. I think the latter is more likely but I have no conclusive evidence.

PLoS Biology: Nanotubes Make Big Science This article reviews work done on TNT's or Tunneling Nanotubes that connect cells that are not in close proximity to each other. It seems to be a mechanism to ensure that cells that need to be together can do so when separated by large distances of up to several cell diameters. To envison developmental biology you have to think like a cell. If you had to connect with a particular cell you could send out diffusible signals but these may not provide the degree of accuracy that you require. In cases requiring greater accuracy, a cell could send out a TNT, connect after utilizing Recognition Factors and then influence the neighboring cell via the transfer of proteins and, apparently, even organelles (see article). One interesting note is that material does not travel within the nanotube--it's not a pipe--but on the surface of the TNT.

So, the cancer cell determines that it is not where it is supposed to be. What does it need to do then? It must free itself from the tissue matrix in which it resides, and it does this by secreting proteases called degradomes, and, this causes the cancer cell to become "unglued" and begin its metastatic journey to other tissues. The CancerDegradome.org website will report on the latest advances in the characterization of these degradomes.

Drug may give cells a fresh start: A chemical could switch adult cells from one type to another. "The cells treated with reversine switched off muscle-related genes and no longer gave rise to muscle cells, suggesting that they had dedifferentiated. When plied with particular chemicals, these cells then appeared to form fat or muscle cells." What I think was happening is that reversine blocked the R factors that the muscle cells were using to establish contact with other cell types. "When plied with particular chemicals . . ." they switched on an earlier phenotype. I wonder what these particular chemicals were and if they could be used clinically to cause cancer cells to switch phenotypes.

Developmental biology: Long-range signalling by touch . This article shows that Recognition factors are on cell membranes and a cell will actually reach out beyond its immediate neighbors to influence development.

Nature Reviews Cancer - Highlights . This article tells how radiation can produce cancer epigenetically by disrupting cell-cell communication. It was once thought that UV light altered DNA (produced mutations) and this caused cancer. But now they are seeing that mutations are not necessary. In line with my theory, the UV radiation altered RF's on the cell surface such that the cells no longer recognized each other and, in trying to re-establish communication, the genome started to express a different set of RF's. If we could determine how many RF's are used in creating an adult organism we would be in a better position to fashion a cure. If it turns out that a great number is involved then we can try to program a cancer cell to change into something like connective tissue. If it's already derived from connective tissue perhaps we can change it into something else that will not be that disruptive to other cells at the metastatic site.

First division seals embryo fate The writer of the article states that, "Mimicking totipotency is the holy grail of stem-cell research. If the underlying molecular signals can be identified, they might be used to transform older cells and tissues, which do not normally repair themselves. Studies such as Zernicka-Goetz's 'begin to provide clues', says Pedersen." This is simply not possible if my theory is correct for the mimicking of totipotency can only result in an embryo. In fact, the writer's next statement contradicts the possibility of the search for the holy grail: The earliest embryonic stages "are very special", he adds, as cells can organize themselves into a complete embryo. Mouse embryonic stem cells used in experiments can be grown in culture only once they have reached the later, blastocyst stage. By this point, they have already lost the ability to self-organize and only form embryos if injected into an existing blastocyst. I...

Squashed embryos switch on genes: Mechanics may guide embryo growth. This article supports my R factor theory but the investigator, Emmanuel Farge, says that his results challenge the notion of a hard-wired development. On the contrary, he merely activated an earlier R factor. Farge, a physicist working at the Curie Institute in Paris, took fruitfly embryos and flattened them at the top. He then saw that a particular gene normally expressed at the bottom of the embryo was now expressed at the top. In line with my theory, pressing on the embryo separated cells and they started expressing an earlier R factor.

This article, in New Scientist , reports on research by microbiologists at the University of California. At first it would seem contradictory (to my theory) that stopping cells from sticking would stop them from becoming cancerous but the R factor is a generic one that is needed by cells to latch on to a neighbor just long enough to "handshake" with that neighbor using a more permanent R factor. The generic R factor is called galectin-3. Think how difficult it would be to type on a computer keyboard if the keyboard were constantly in motion. You would have a very difficult time communicating and so would the cell trying to handshake using specific R factors. Why would eliminating the generic glue help to eradicate the cancer? I think that this generic binding is the first step in cell recognition and without it the cell does not go on to express its entire repertoire of R factors. Expressing a single R factor would mean that immune cells now have the opportunity to loca...

I apologize for that last post. I was testing my new Google bar with a Blogger button on it. I'd like to elaborate on an aspect of cancer that supports my theory of cancer. If you look at the various kinds of cancer, you will note that the most common cancers are those where the cells are in direct contact with an often toxic environment or have a high replication rate; namely, skin and GI tract and lung. The least common cancers are those where cells--and their R factors--are protected against environmental damage or have a low replication rate; namely brain and bone and other specialized tissues. Why is the environment and replication important? The environment hits cells with chemicals, radiation, trauma, and viruses that interfere with R factor function either directly or via DNA damage or alteration. With regard to replication, a cell that is not replicating will not expose R factors to damage (they are always 'shaking hands,' so to speak) and it will not activate ...

Proofreading, data-entry, transcription, and backup services