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Beta-catenin Overexpressed in Skin Cancer

[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
Recent posts

The Cell Recognition Factor Theory is Fast Heading Towards Vindication

"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

Republishing my First Blog Because Blogger Refuses to Alter Chronological Order

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...

Cancer in Microgravity

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.

Biological Pathways Symbology

St. Peregrinus and CRF Theory

[ 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...

What about the unattached cell?

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...