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Gene polymorphisms and pharmacogenetics in rheumatoid arthritis.

Rego-Pérez I, Fernández-Moreno M, Blanco FJ - Curr. Genomics (2008)

Bottom Line: The advent of new biological agents, as well as the more traditional disease-modifying antirheumatic drugs, has resulted in highly efficient therapies for reducing the symptoms and signs of RA; however, not all patients show the same level of response in disease progression to these therapies.These variations suggest that RA patients may have different genetic regulatory mechanisms.The extensive polymorphisms revealed in non-coding gene-regulatory regions in the immune system, as well as genetic variations in drug-metabolizing enzymes, suggest that this type of variation is of functional and evolutionary importance and may provide clues for developing new therapeutic strategies.

View Article: PubMed Central - PubMed

Affiliation: Osteoarticular and Aging Research Lab, Genomic Unit, Rheumatology Division, Juan Canalejo Hospital, Xubias 84 15006- A Coruña, Spain.

ABSTRACT
Rheumatoid arthritis (RA) is a systemic, chronic and inflammatory disease of unknown etiology with genetic predisposition. The advent of new biological agents, as well as the more traditional disease-modifying antirheumatic drugs, has resulted in highly efficient therapies for reducing the symptoms and signs of RA; however, not all patients show the same level of response in disease progression to these therapies. These variations suggest that RA patients may have different genetic regulatory mechanisms. The extensive polymorphisms revealed in non-coding gene-regulatory regions in the immune system, as well as genetic variations in drug-metabolizing enzymes, suggest that this type of variation is of functional and evolutionary importance and may provide clues for developing new therapeutic strategies. Pharmacogenetics is a rapidly advancing area of research that holds the promise that therapies will soon be tailored to an individual patient's genetic profile.

No MeSH data available.


Related in: MedlinePlus

Molecular mechanism of biologic therapies: A) The tumor necrosis factor-α (TNF-α) blocker, Etanercept. B) The tumor necrosis factor-α (TNF-α) blocker, Infliximab. C) The tumor necrosis factor-α (TNF-α) blocker, Adalimumab. D) The interleukin-1 (IL-1) blocker, Anakinra, a recombinant form of the human IL-1 receptor antagonist (IL-1RA).
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Figure 2: Molecular mechanism of biologic therapies: A) The tumor necrosis factor-α (TNF-α) blocker, Etanercept. B) The tumor necrosis factor-α (TNF-α) blocker, Infliximab. C) The tumor necrosis factor-α (TNF-α) blocker, Adalimumab. D) The interleukin-1 (IL-1) blocker, Anakinra, a recombinant form of the human IL-1 receptor antagonist (IL-1RA).

Mentions: Etanercept is a dimeric fusion protein that joins the human p75 TNF receptor to the FC domain of human IgG1 (Fig. 2a). This drug is made exclusively of human amino acidic sequences and has 934 amino acids.


Gene polymorphisms and pharmacogenetics in rheumatoid arthritis.

Rego-Pérez I, Fernández-Moreno M, Blanco FJ - Curr. Genomics (2008)

Molecular mechanism of biologic therapies: A) The tumor necrosis factor-α (TNF-α) blocker, Etanercept. B) The tumor necrosis factor-α (TNF-α) blocker, Infliximab. C) The tumor necrosis factor-α (TNF-α) blocker, Adalimumab. D) The interleukin-1 (IL-1) blocker, Anakinra, a recombinant form of the human IL-1 receptor antagonist (IL-1RA).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2691664&req=5

Figure 2: Molecular mechanism of biologic therapies: A) The tumor necrosis factor-α (TNF-α) blocker, Etanercept. B) The tumor necrosis factor-α (TNF-α) blocker, Infliximab. C) The tumor necrosis factor-α (TNF-α) blocker, Adalimumab. D) The interleukin-1 (IL-1) blocker, Anakinra, a recombinant form of the human IL-1 receptor antagonist (IL-1RA).
Mentions: Etanercept is a dimeric fusion protein that joins the human p75 TNF receptor to the FC domain of human IgG1 (Fig. 2a). This drug is made exclusively of human amino acidic sequences and has 934 amino acids.

Bottom Line: The advent of new biological agents, as well as the more traditional disease-modifying antirheumatic drugs, has resulted in highly efficient therapies for reducing the symptoms and signs of RA; however, not all patients show the same level of response in disease progression to these therapies.These variations suggest that RA patients may have different genetic regulatory mechanisms.The extensive polymorphisms revealed in non-coding gene-regulatory regions in the immune system, as well as genetic variations in drug-metabolizing enzymes, suggest that this type of variation is of functional and evolutionary importance and may provide clues for developing new therapeutic strategies.

View Article: PubMed Central - PubMed

Affiliation: Osteoarticular and Aging Research Lab, Genomic Unit, Rheumatology Division, Juan Canalejo Hospital, Xubias 84 15006- A Coruña, Spain.

ABSTRACT
Rheumatoid arthritis (RA) is a systemic, chronic and inflammatory disease of unknown etiology with genetic predisposition. The advent of new biological agents, as well as the more traditional disease-modifying antirheumatic drugs, has resulted in highly efficient therapies for reducing the symptoms and signs of RA; however, not all patients show the same level of response in disease progression to these therapies. These variations suggest that RA patients may have different genetic regulatory mechanisms. The extensive polymorphisms revealed in non-coding gene-regulatory regions in the immune system, as well as genetic variations in drug-metabolizing enzymes, suggest that this type of variation is of functional and evolutionary importance and may provide clues for developing new therapeutic strategies. Pharmacogenetics is a rapidly advancing area of research that holds the promise that therapies will soon be tailored to an individual patient's genetic profile.

No MeSH data available.


Related in: MedlinePlus