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자료유형
학술저널
저자정보
Fatıma Ceren Tuncel (Department of Medical Biology Faculty of Medicine Institute of Health Sciences Istanbul University) Istemi Serin (Department of Hematology Istanbul Training and Research Hospital University of Health Sciences Ista) Sacide Pehlivan (Department of Medical Biology Faculty of Medicine Institute of Health Sciences Istanbul University) Yasemin Oyaci (Department of Medical Biology Faculty of Medicine Institute of Health Sciences Istanbul University) Mustafa Pehlivan (Department of Hematology Faculty of Medicine Gaziantep University Gaziantep Turkey)
저널정보
대한혈액학회 Blood Research Blood Research Vol.57 No.4
발행연도
2022.12
수록면
250 - 255 (6page)
DOI
10.5045/br.2022.2022097

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Background The suppressor of cytokine signaling-1 (SOCS-1) functions to induce an appropriate immune response and is an essential physiological regulator of interferon signaling. DNA methylation involves adding a methyl group to the carbon 5 position of cytosine. Besides comparing SOCS-1 gene methylation status between patients with multiple myeloma (MM) and healthy controls, this study also aimed to demonstrate the effect of SOCS-1 gene distribution and the effect of methylation of SOCS-1 on progression-free survival (PFS) and overall survival (OS). Methods This study included 120 patients diagnosed with MM between January 2018 and 2020 and 80 healthy individuals. The distribution of the SOCS-1 genotypes was statistically compared between MM patients and healthy controls. Additionally, the statistically significant effects of these genotypes on survival were examined. Results The CA/CA genotype of SOCS-1 was significantly higher in healthy controls (P=0.001), while the Del/Del genotype was significantly higher in patients with MM (P =0.034). The percent methylated reference (PMR) value of the SOCS-1 gene was significantly higher in the healthy controls (median, 43.48; range, 2.76‒247.75; P=0.001). Patients with a PMR value of ≥43.48 were 3.125 times more likely to develop progression than those with a PMR value of <43.48. Conclusion The effects of SOCS-1 polymorphisms on the pathogenesis of MM and SOCS-1 methylation will further shed light on the pathophysiology of MM.

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