26.3 Personalized Medicine

359

A more powerful multiomics (gene expression and DNA methylation) approach

was later used to reveal the signalling factors active in inflammatory comorbidities. ¹⁵

Chronic kidney disease (CKD): molecular mechanisms were sought by determin-

ing the DEGs in various types of CKD, ¹⁶ the transcriptomes of which had been

determined using microarrays. The DEGs were further analysed using gene ontol-

ogy and pathway enrichment analysis and protein–protein interaction networks were

constructed; hundreds of genes and their regulatory networks could be identified.

This knowledge can be useful for selecting biomarkers and suggesting therapeutic

approaches.

Cancer bioinformatics is an active field. Some examples of work targeted onto

clinical applications are the use of proteomics to identify biomarkers, which may aid

in diagnosis; ¹⁷ and continuing efforts to find somatic mutations in cancer genomes. ¹⁸

26.3

Personalized Medicine

Personalized medicine (or precision medicine as it is sometimes called—but this can

also mean keyhole surgery, microsurgery and the like; and drugs that are so well

targeted that systemic dosing can be avoided) can mean at least two things: adjusting

drug type and dose to an individual patient’s phenotype; and adjusting therapy to

individual patient’s genome or genotype. The latter can mean both gene and stem

cell therapy.

Obviously a patient’s phenotype encompasses any ailment, and is taken into

account in an integrative, intuitive way by the physician when prescribing treatment.

There is a spectrum of personalization; mass medication is impersonal (although

there are always ways for an individual to escape from it). Examples are the fluori-

dation of tap water, ¹⁹ or compulsory vaccination. It impinges on what are considered

to be fundamental human rights and is, therefore, unethical; at the very least those

responsible for such interventions need to robustly justify why such considerations

should be set aside. Ingestion of iodine tablets distributed after a nuclear accident is

voluntary, which is an essential attribute of any medical treatment.

Given the prevalence of serious adverse drug reactions, there is much interest

in identifying genetic risk factors for them, which would enable their elimination,

provided that appropriate genetic screening had been carried out on the patient. ²⁰

15 Xiao et al. (2018).

16 Zhou et al. (2018).

17 Oh et al. (2011).

18 Kim et al. (2013).

19 Cross (2015).

20 Many of these adverse reactions, which are closely related to susceptibility to toxins, can be

traced to variation in an individual’s cytochrome P450 enzymes, which are strongly involved in

drug metabolism (Zanger and Schwab 2013).