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Tchetina E, Markova G. The clinical utility of gene expression examination in rheumatology. Mediterr J Rheumatol. 2017;28(3):116-126doi: 10.31138/mjr.28.3.116.
Tchetina, E., & Markova, G. (2017). The clinical utility of gene expression examination in rheumatology. Mediterranean journal of rheumatology, 28(3), 116-126. https://doi.org/10.31138/mjr.28.3.116
Tchetina, Elena, and Markova, Galina. "The clinical utility of gene expression examination in rheumatology." Mediterranean journal of rheumatology vol. 28,3 (2017): 116-126. doi: https://doi.org/10.31138/mjr.28.3.116
Tchetina E, Markova G. The clinical utility of gene expression examination in rheumatology. Mediterr J Rheumatol. 2017 Sep 29;28(3):116-126. doi: 10.31138/mjr.28.3.116. eCollection 2017 Sep. PMID: 32185269; PMCID: PMC7046055.
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Mediterr J Rheumatol. 2017 Sep 29;28(3):116-126. doi: 10.31138/mjr.28.3.116. eCollection 2017 Sep.

The clinical utility of gene expression examination in rheumatology.

Mediterranean journal of rheumatology

Elena Tchetina, Galina Markova

Affiliations

  1. Immunology and Molecular Biology Laboratory, Nasonova Research Institute of Rheumatology, Moscow, Russia.

PMID: 32185269 PMCID: PMC7046055 DOI: 10.31138/mjr.28.3.116

Abstract

Rheumatoid arthritis (RA) is a chronic inflammatory disease with unknown etiology that affects various pathways within the immune system, involves many other tissues and is associated with pain and joint destruction. Current treatments fail to address pathophysiological and biochemical mechanisms involved in joint degeneration and the induction of pain. Moreover, RA patients are extremely heterogeneous and require specific treatments, the choice of which is complicated by the fact that not all patients equally respond to therapy. Gene expression analysis offer tools for patient management and personalization of patient's care to meet individual needs in controlling inflammation and pain and delaying joint destruction.

© 2017 The Mediterranean Journal of Rheumatology (MJR).

Keywords: TNFα; gene expression; pain molecular markers; proteases; response to therapy; rheumatoid arthritis; type I IFN-response genes

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