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New Developments in the Pharmacogenetics of Psoriasis: 
HLA-Cw6 as a Marker for the Treatment of Psoriasis with Biological Therapies

Antonio Costanzo, MD, Giulia Spallone, MD, Marina Talamonti, MD, 
Elisabetta Botti, MD, and Sergio Chimenti, MD

Pharmacogenomics is the branch of pharmacology that studies the genetic mechanisms of the individual variations in the response to xenobiotics and, more particularly, to drugs. It includes the discipline of pharmacogenetics, which aims to identify variations in the genome that are responsible for alterations in the response of the organism [1]. Of the three billion bases in the human genome, 99.7% are identical between individuals. The variations or polymorphisms of the remaining 0.3% of the genome represent approximately one million nucleotides that differ, and these form the basis of the differences between individuals. Until recently, only a very small fraction of the human genome and its variations were defined. However, with the availability of novel methods in molecular biology, it has become possible to investigate the whole genome and all of its variations [2]. Variations or specific substitutions of only one nucleotide are called single nucleotide polymorphisms (SNPs), and are all identifiable. By comparing particular areas of DNA between several individuals having a common pathology (psoriasis for example) with those of people who do not have the disease, it is possible to locate SNPs that correlate with the studied disease. These SNPs are not necessarily responsible for the disease. They can be genetic markers that are located close to the genes causing the disease. Of course, SNPs can also occur within coding or regulatory regions of a gene, directly affecting the function or expression of its product. For example, functional polymorphisms have been found in the genes coding for enzymes involved in the metabolism of drugs, in those coding for receptor targets of drugs, or in genes encoding drug transporter molecules. These variations can often be associated with a reduction in the activity of the encoded protein, resulting in higher toxicity or inefficiency of a drug.

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