Clinical OMICS

MAY-JUN 2018

Healthcare magazine for research scientists, labs, pathologists, hospitals, cancer centers, physicians and biopharma companies providing news articles, expert interviews and videos about molecular diagnostics in precision medicine

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News www.clinicalomics.com May/June 2018 Clinical OMICs 3 S tudies by researchers at the Univer- sity of Michigan, Ann Arbor, have uncovered a mechanism by which a particular variant of the HLA-DRB1 allele and exposure to environmen- tal pollutants such as cigarette smoke or vehicle exhaust work together to increase rheumatoid arthritis (RA) risk and the severity of bone damage in patients with the disease. "We found a particular enzyme that acts as a channel, or pathway, in the cell for a conversation between the two culprits, so they work together to do greater damage," said research lead Joseph Holoshitz, M.D., professor of internal medicine and associate chief for research at the University of Mich- igan School of Medicine's Division of Rheumatology. "Individually they are bad, but together, they're worse." Reporting on their in vitro and in vivo studies in the Proceedings of the National Academy of Sciences, the University of Michigan team and collaborators at the University of Ten- nessee Health Science Center suggest that their findings could lead to the development of drugs that block the gene-activated pathway and so reduce the incidence of RA and severity of bone damage. About two-thirds of RA risk is attributed to genes, and the single most significant genetic risk factor for RA is the shared epitope (SE), a five- amino-acid sequence motif encoded by the RA-associated HLA-DRB1 alleles, the researchers explained. But RA isn't all down to genes. Environ- mental factors also influence RA sus- ceptibility. The autoimmune disease is associated with exposure to environ- mental pollutants such as dioxin-like compounds and tobacco smoke, and RA is more prevalent in urban popula- tions and among people who live near highways, irrespective of whether or not they smoke cigarettes. Recent evidence also suggests that genes and environment may work together to further increase the risk of RA, such that the likelihood of developing the disease is "signifi- cantly amplified in genetically sus- ceptible individuals who have been exposed to various environmental pollutants." Cigarette smoke, for example, "increases the disease risk of SE-positive individuals in a multipli- cative, dose-dependent fashion," the researchers pointed out. What scien- Pollution and Genes Work Together to Increase Severity of Rheumatoid Arthritis By Sophia Ktori JodiJacobson / Getty Images (continued on next page)

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