Skip to main content
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.

Comments

Popular posts from this blog

Biological Pathways Symbology

Mutations

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...

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...