Ribonoscopy and Personalized Medicine - Molecular Theory of the Living Cell - page 591

The emergence of personalized medicine over the past decade or so has been
strongly motivated by the revolutionary developments in the so-called omics in
basic biological sciences throughout the second half of the twentieth century and
the first decade of the twenty-first century. The development of personalized
medicine is now officially endorsed by the Obama Administration. Early in 2010,
Dr. M. Hamburg, FDA Commissioner, “announced a new partnership with the
National Institutes of Health that is designed to more quickly get scientific and
medical breakthroughs in personalized medicine, among other fields, into clinical
practice” ( Personalized Medicine Coalition Newsletter , Spring, 2010, p. 8).
Omics is defined as the genome-wide studies of genes ( genomics ), transcripts
( transcriptomics ), proteins ( proteomics ), and metabolites ( metabolomics ).
Transcriptomics, the study of genome-wide alterations of RNA levels inside the
cell, is often omitted in defining personalized medicine, but I predict that
transcriptomics will play a major role in drug discovery research and personalized
medicine because RNA molecules can serve as convenient intracellular reporter
molecules whose behaviors can be easily monitored using ribonoscopy (Sect.
12.8.2 ). Another component not included in the current definition of personalized
medicine is intracellular (ic) dissipative structures or ic-dissipatons (Sect. 12.5 ) such
as the patterns of the changes in RNA levels and RNA sequences that can be used to
differentiate subtypes of cancer cells (for a recent review, see van't Veer and Bernards
2008). As can be seen in the Bhopalator models of the living cell (Fig. 2.11 )and
biological evolution (Fig. 14.7 ) , all intracellular processes involving genes, RNAs,
proteins, and metabolic pathways eventually converge to generate various
ic-dissipatons , which are postulated to be synonymous with cell functions (see
Sect. 10.2 ). For convenience, the study of genome-wide ic-dissipatons may, therefore,
be referred to as ic-dissipatonics, in analogy to “electronics,” the study of electrons.
The molecular theory of the living cell developed in this topic can provide the
theoretical framework for developing personalized medicine as defined in Fig. 18.3 .
The other side of the personalized-health coin is personalized pathology , and
according to Fig. 18.3 , personalized pathology can arise in five distinct ways - due to
the failure of any one of the cellular components belonging to genomics (G),
transcriptomics (T), proteomics (P), metabolomics (M), or ic - dissipatomics (D),
whichever happens to be the weakest link , W, in the complex network of molecular
interactions constituting the living cell under a particular environmental condition.
If we express the stability of the weakest ic-dissipatons in diseased cells as P(D)
(the more stable the ic-dissipatons, the higher would be the probability of finding
that dissipations), where P(D) is determined by the probability of the weakest G, T,
P, or M, depending on the health condition of the patient, we can express the death
rate , d, of individuals from the disease under consideration as in Eq. 18.4 in analogy
to the death-rate equation discussed in the context of the MTLC-based model of
evolution, Eq. 14.40 :

d ¼ d 0 1 ½ PD ðÞ (18.4)