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attribute the changes in the level of an RNA level as resulting only from the
structural gene encoding it.
2. In multicellular organisms, one gene can code for up to 38,016 mRNAs through
alternative splicing (Schmucker et al. 2000) (see Row 5 in Table 19.3 ). Thus, it is
highly unlikely that all of the proteins encoded in a given gene contribute to only
one phenotype and hence it would be impossible to infer the gene responsible for
a phenotype (such as breast tumor) from observing that an RNA molecule is
associated with that phenotype.
Finally, the object of discovery by the currently fashionable approach in
microarray data analysis, that is, genes, are equilibrium structures ( equilibrons ),
whereas the objects sought after by ribonoscopy is ribons, which are dissipative
structures ( dissipatons ) (see Row 7 in Table 19.3 ). As pointed out in Sect. 3.1.5 ,
equilibrons and dissipatons belong to the two different categories of structures.
As is clear from the above discussions, the ribonoscopic strategy for discovering
drug targets being advanced here is based on the idea that dissipative structures (or
dissipatons ) (Sect. 3.1 ) are the ultimate targets of drugs in contrast to the traditional
view which regards equilibrium structures (equilibrons) as drug targets. The new
idea can be expressed in several equivalent ways:
The ultimate targets of all drugs are the dissipative structures of the living cell or
ic-dissipatons. (19.2)
No therapeutic nor toxic effects can be exerted by any agent without affecting cell functions
or ic-dissipatons. (19.3)
It is impossible for an agent to be therapeutically effective unless it can affect cell functions,
i.e., ic-dissipatons.
(19.4)
We may refer to any of Statements 19.2-19.4 as the First Law of Theragnostics .
According to Bloomberg Business Week (as reported in Personalized Medicine
Coalition Members Newsletter , spring 2010, p. 12), FDA Commissioner
Dr. Margaret Hamburg said in February, 2010 that
diagnostic tests based on biomarkers will make it possible for drug companies to salvage
data from unsuccessful clinical trials by resubmitting drugs for approval for smaller subsets
of patients. (19.5)
Statement 19.5 by Dr. Hamburg encourages the development of biomarker-
based diagnostic tools for which ribonoscopy, armed with a comprehensive molec-
ular theory of the living cell, may play an essential role in the coming decades.
The ribonoscopic method of drug target discovery is different from the traditional
method at several levels (in addition to the differences listed in Table 19.3 ). The
ribonoscopic method allows discovering both pure compounds and mixtures
of compounds as potential drug candidates, since, in principle, both types of substances
can “flatten” the difference ribonic spectra (see Panels c and d, Fig. 19.4 ). In other
words,
Unlike the traditional method of drug discovery which is limited to pure compounds,
the ribonoscopic method can identify both pure compounds as well as compounds
consisting of two or more known or unknown chemicals as drug candidates.
...
(19.6)
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