Could the loss of regulation of genetic expression in cancer cells be used to cause their necrosis?
In cancer cells the control over the genetic message involved in the induction of mitosis is irreversibly lost. This fact is indicated by certain phenomena displayed by cancer cells under restricted nutritional conditions. Cells transformed by DNA viruses (which stabilize "p53") keep on cycling and die. In starving cells at the inside of tumors the synthesis of pre-rRNA still proceeds while all other anabolic processes are already at a standstill. The reason is that glutamine, glycine and aspartate are channelled into the enzymatic pathways for the synthesis of nucleosides: thus, protein synthesis is denied those aminoacids. Such situations might be imitated through the administration of excess nucleosides and (within limits) the simultaneous restriction of some selected aminoacids. DNA replication depends on the stabilization of p53, but an accumulation of pre-rRNA might occur, which ultimately might be harmful for cancer cells. Several ways to improve this rationale might be tested on cultured cells and on research animals. They include the destruction of methionine with bacterial enzymes, or the addition of ornithine, a precursor of putrescine, which is an important factor of DNA and pre-rRNA synthesis.
D000596:Amino Acids / Q000378:metabolism; D002455:Cell Division; D002471:Cell Transformation, Neoplastic; D006706:Homeostasis; D006801:Humans; D008938:Mitosis; D009336:Necrosis; D009369:Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D009705:Nucleosides / Q000378:metabolism
D000596:Amino Acids; D009705:Nucleosides