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...
A theory created to explain the fact that cancer cells turn back to normal when put in an embryo; it's called the cell recognition theory of cancer. Basically, a cell loses touch with its neighbor(s)or with the ECM. This releases the physical constraints on the nucleus which then cycles through earlier embryonic stages hoping to establish contact once again (it partially succeeds when it establishes a metastasis).
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