Cancer Theory

[I've taken the plunge and bought myself an online subscription to Nature and 50+ other publications they produce. This will mean more posts on this blog] This is a quick read. The researchers found that beta-catenin was over-expressed in skin cancer while in normal stem cells, it is only expressed periodically. This falls inline with the CRF theory. Beta-catenin is an essential player in how the cell reprograms itself by implementing epigenetic changes. Clearly, a cancer cell, having difficulty establishing contact with the proper CRF's, might continue to express beta-catenin because the embryonic CRF's are nowhere to be found.   Baker, M. Skin cancer needs beta-catenin. Nat Rep Stem Cells (2008). https://doi.org/10.1038

"The authors concluded that human colon-cancer stem cells are defined not by their intrinsic gene-expression patterns, but by their location." "if these same cells are removed from adult tissues, they quickly reactivate multipotency, or the ability to differentiate into discrete cell types, including cancerous ones, reinforcing the tissue environment’s crucial role in tumor development." "...suggesting that the tissue environment plays a part in defining stem cells." https://www.nature.com/articles/d41586-021-01029-4?utm_source=Nature+Briefing&utm_campaign=908962649e-briefing-dy-20210421&utm_medium=email&utm_term=0_c9dfd39373-908962649e-45862826

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...

[ 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...

While this procedure is not what I had in mind when I spoke of being able to reprogram the cancer cell, I'm nevertheless glad that reprogramming was found to be possible for the unattached cancer cell. The unattached immune cell is needed everywhere in the body and it would make sense for a cancer derived from an immune cell to differentiate into other immune cells as needed. This is what was found by the Stanford researchers--reprogramming of leukemia cells into normal granulocytes and macrophages via supplied ligands or transcription factors. The initial observation from Stanford came about as a result of a shotgun approach. This approach should also be used for the solid tumor and if their cocktail doesn't do it, I would consider extracting Embryonic Cell Surface molecules from various developmental time points. Finding the right CRF for the differentiation of  solid tumors is right around the corner. My next post will be one showing what the CRF theory helps explain wh...

Researchers engineer a switch to tame aggressive cancers Quoting from the ScienceDaily article: "Certain proteins, such as E-cadherin, are important for the maintenance of normal tissue structure. When tumors become more aggressive, they often lose E-cadherin, resulting in dramatic changes to their structure, function and ability to spread. But when cancer cells are forced to express E-cadherin, research suggests they behave less aggressively and revert back to normal." And, "'Although genomics technology has revealed many new proteins that could force cancers to 'switch' back to their less aggressive state, these new targets have not yet been validated in preclinical models like mice because it is difficult to determine the molecular effects on each individual cancer cell, Dr. Lewis says.'" Cadherin and catenin mechanisms have been at the top of my list of possible candidates for the Cell Recognition Factor whose malfunction or disassociation and do...

This post is based on speculation. It is an attempt at explaining the prevalence of mutations in cancer and their role in perpetuating the cancerous state. The transcriptome of a cell may be classified into two sets: embryonic and adult. There are, of course, conserved elements that form a union of these sets but we are more interested in the embryonic transcriptome exclusive of the union. We now consider the two Nucleotide Excision Repair (NER) mechanisms that have been studied to date: Global Genomic Repair (GGR) and transcription-coupled repair (TCR). Atanassov, et.al. A mutation can take place at or near an adult transcriptome and it is usually repaired by TCR. However, if a mutation takes place at an embryonic transcriptome during the adult stage , TCR can not repair it and, because it is in the adult, GGR may not be able to effect repairs. According to Lans et.al., "Intriguingly, in juvenile and adult animals TCR is the major NER pathway involved in the UV response. Analysi...

In a recent op-ed piece in the NY Times , James D. Watson makes several statements on cancer that need to be addressed by this writer. First, he states that cancer can be beat because we now know the genetics and chemistry of the cancer cell. In line with what I have written so far, the present knowledge on cancer genetics will not lead to a cure. We need to know the steps that the epithelial cells go through from from embryonic stem cells to differentiated cells. Only this will enable us to recreate the embryonic milieu that the cancer cell seeks. He goes on to say that, "We shall soon know all the genetic changes that underlie the major cancers that plague us." This knowledge will not help us unless it includes CRF's or those cell surface factors that guide cells to their next station in the fully developed organism. [ I know I promised to look into possible contenders for these molecules but after reading the only molecular chemistry literature that I could get my hand...

Researchers are still trying to use embryonic stem cells (ES) to cure disease and continue to encounter tumor formation. A recent study did something along the right lines when it co-transplanted bone marrow stem cells (BMSC)along with ES. There were no tumors formed during the 5 weeks of the study. To me, this indicates that the BMSC had started to revert back to ES and these provided the CRF's required by the original ES to prevent them from forming tumors. What needs to be done is to search for CRF's in embryonic tissues. The main difficulty here is which of the hundreds of molecules on the cell surface are CRF's. I am working on trying to identify candidates for this role. One that caught my eye was the SSEA or stage-specific embryonic antigen because this theory requires that there be stage specificity. A candidate that I focused on back in the 70's when I first came up with the CRF theory were the glycoconjugates simply because they play a role in such phenomena a...

How would you go about reprogramming cancer cells back to normalcy? You would first identify the most likely candidate(s) for Cell Recognition Factor(s) and determine how they change during the development of, let's say, a pancreatic cell. From the time of the first egg mass to mature adult cell, what CRF's were being expressed? Take these and chemically attach them to a carrier that is able to diffuse through tissue. Inject the complex into the blood or lymphatic system. Repeat the cocktail until normalcy is achieved. Once we know the exact sequence that particular CRF's are expressed, we can just inject stage-specific CRF's in a particular sequence. A difficulty that I'm hoping does not present itself is that of individual variations in CRF's. We may not want to have to design a sequence on an individual basis. It would be much better, at least initially, if one sequence for differentiation of pancreas cells was the same for all individuals. Essential elements...

I'd like to address an issue which is not that well-resolved in my mind. That is, do cancer cells arise from any cell of the body or only from stem cells? I believe that differentiated cells are subject to the Hayflick limit and, as such, will self-destruct (apoptosis) if they are unable to establish contact with the pre-assigned cell neighbors. But stem cells have built-in immortality. (I wish I had a subscription or access to journals so that I can cite the literature for every point I make. Unfortunately, I have to rely on the media to bring me news of new developments) That immortality may be checked by what are called Natural Killer Cells but if a stem cell should lose contact and start to reprogram it's phenotypic expression before NKC's have had a chance to stop them, they will begin to express one CRF after another and thereby avoid detection just like a parasite would do. Perhaps a little graphics is in order. You are a cell. You reach out with molecules similar to...

This article was recently published in PLOS. This is a great scientific publishing medium that doesn't charge anyone a cent to read their stuff, unlike Science and Nature and the others that hoard their publications at the expense of humanity. Anyway, the article points out that a boy being treated with stem cells for a rare genetic condition developed tumors of the brain and spinal cord. These results should come as no surprise for readers of this blog. The cells injected into the nerve tissues were allografts--they were obtained from a source other than the patients own tissues. These clearly will not be at home in another person's body and they will begin to express embryonic Cell Recognition Factors in the hope that they could establish communication. As we have learned here, a cell must know exactly where it is. Such communication must exist. If it does not, it would mean that A) any manner of invader could easily make its home in another multicellular organism, or B) any...

A researcher has found a way to show embryonic development in great detail. He has movies that show hordes of disconnected cells moving to opposite poles of the early embryo. This mass migration shows that cells react to chemical agents that diffuse throughout the tissues and it runs counter to what I've been saying about CRF's. It should be noted, however, that early on cells need to reproduce rapidly and take positions that are not too specific. This is done so that many tissues can start their development simultaneously. You will still see mass migrations occuring after the formation of the three germ layers but you will also start to see more and more cohesive behavior.

Every good theory needs to make accurate predictions. As such, I predict the following. 1. If you take the full gamut of embryologic TSA's (tissue specific antigens) and, either alone or attached to some mobile substrate, put them in contact with cancer cells, you will cause the reprogramming of the cancer cell's genomic expressions. 2. There is a particular sequence of TSA's that will take any given cancer cell to normalcy. 3. The particular sequence could be individual specific for, if you had them species-wide, it would be easy for a parasite to mimic them and avoid detection by immune cells. Instead, parasites normally continuously express a wide range of antigens throughout their life. 4. Cancer could be induced by denaturing the TSA's continuously. 5. The rate of cancer is directly proportional to the rate of cell division because this allows for a greater probability for the TSA's to become denatured. 6. Putting cancer cells into an embryo will result in the ...

University of Florida (2007, May 26). Stem Cells May Look Malignant, Not Act It . ScienceDaily . Retrieved December 13, 2007, from http://www.sciencedaily.com­ /releases/2007/05/070523134908.htm This article goes back 6 months but I just noticed it in one of my feeds. It is not clear who the population is exactly but some cancer patients have cancers that also contain normal bone marrow stem cells. They are normal in the sense that they are not malignant but abnormal because they no longer look like bone marrow cells. It was stated that several patients had had bone marrow transplants. Here is what I think is happening: bone marrow cells escape the bone marrow primarily through the opening that is made in the bone in order to deposit the cells. (it was reported that, prior to receiving the cells, the patients had radiation and/or chemo in order to stop the rejection process. This pretreatment is known to cause cancer in some patients.) However, even with preexisting cancer, the bone m...

I heard some real exciting news about a researcher that had managed to get adult stem cells to go embryonic. It was touted as a great way to get stem cells without having to sacrifice embryos. Yes, but I like it because we may be able to get cancer to revert to normal by taking a patient's stem cells, making them go embryonic, and places those cells in contact with the patient's cancer cells. If you've been following my blog, you know that cancer cells may just be looking for the right neighbors that will reset their genome to normalcy. The right "neighbors" are those that, like cancer cells themselves, express embryonic CRF (cell recognition factors).

The diffraction limit has been overcome by engineers at harvard. Now for the first time we will be able to view a cell surface in all its glory. Previously, we were able to view the cell surface with the electron microscope but the preparation techniques denatured the proteins. Now, however, we will soon be able to use an optical microscope to view objects in the 100 nanometer range and below. Education is a two-edged sword. I remember hearing about the diffraction limit and coming to the conclusion that we would never be able to view the cell surface in an unaltered state. Indeed, you must always take everything you learn with a grain of salt. What does this mean with regard to progress in Cell Recognition Factors? For one thing, we will be able to demonstrate the importance of cell recognition in development. And speaking of development, we may, in our lifetime, be able to manufacture a cell sorting machine that can recognize adult stem cells and pluck them out for further study. Wh...

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.