Saturday, February 19, 2011

Can Oncotherapeutic (Anticancer) Mechanomers Be Mechanomerically Selected?

Mechanomers toxic to cancer cells but not to cells of their parent (or other normal) types can be mechanomerically selected, for the individualized oncotherapies or idiotherapies necessitated by the individualized nature of cancers.

Cancer cells are mutated cells, with at least one and usually multiple abnormal biopolymers (DNAs, messenger RNAs and proteins), and the differences between such biopolymers and their normal parent biopolymers will allow the mechanomeric selection of mechanomers which are toxic to such cells only (e.g., lethal enzymes activated by complexing with such abnormal biopolymers only).

At its simplest, such selection will take the form of parallel matricial mechanomeric selection: overlaying a set of parallel identical replicated random mechanomer matrices with, respectively, a culture of the cancer cells in question, perhaps a culture of the parent cell-type of that cancer, and cytopalette cultures of as many other (normal) cell types generated and cultured from the patient as practicable; observing for regions where on the first matrix the cancer cells die but on the others none do, deaths signaled by mechanomeric indication for greatest sensitivity; extracting the random mechanomers from those regions from yet another parallel matrix; re-matriciating the mechanomers from each such region using different media to separate them; and repeating, until a set of individualized antineoplastic or oncotherapeutic mechanomers is selected.

It is unlikely that even with the use of multiple oncotherapeutic mechanomers that all the cells of a cancer will be killed, and indeed some if not most cancers more or less steadily mutate, so the mechanomeric oncotherapies of such cancers will therefore involve not only multiple mechanomers but also one or more extra passes or rounds of such multiplex therapy, as the cancer reoccurs to be re-sampled and a new set of oncotheraputic mechanomers selected to deal with it, with the majority of such cells destroyed by each pass, and a genetically-different minority left (if any) to begin again (note that even if not directly destroyed, the cells of such cancer held in check long enough should become ever more mutated, function ever more poorly, with ever greater numbers of its cells being fatally mutated, or exhibiting mutated biopolymers detectable and those cells therefore destroyed by the immune system, in "neoplastic burnout").

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