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The clinical signature of genetic variants and serum levels of macrophage migration inhibitory factor in Egyptian breast cancer patients

巨噬细胞移动抑制因子 乳腺癌 基因分型 医学 发病机制 免疫学 等位基因 内科学 癌症 基因型 细胞因子 肿瘤科 生物 基因 遗传学
作者
Mahmoud A. Seliem,Ahmed M. Mohamadin,Mohamed I. Kotb El-Sayed,Yahia Ismail,Ahmed A. El-Husseiny
出处
期刊:Breast Cancer Research and Treatment [Springer Science+Business Media]
卷期号:208 (1): 57-66
标识
DOI:10.1007/s10549-024-07393-9
摘要

Abstract Purpose Macrophage migration inhibitory factor (MIF) is an integral cytokine for the modulation of both innate and adaptive immunity and is involved in the pathogenesis of various cancers. However, conflicting findings on the relationship between MIF polymorphisms and breast cancer (BC) have been reported in earlier research. We investigated the clinical value of serum MIF levels and the association between MIF rs1049829 and rs755622 variants with their serum levels and propensity to develop BC. Methods A total of 133 treatment-naïve Egyptian BC females and 126 apparently healthy controls were matriculated in this case–control study. The serum MIF protein levels were quantified by ELISA, whereas the genotyping was executed utilizing the TaqMan® allelic discrimination assay. Results A significant increase in the serum MIF level in BC cases was observed in comparison to control subjects ( P < 0.0001), with a diagnostic potential to discriminate BC with 92.5% sensitivity and 73.7% specificity at a cut-off value > 9.47 ng/mL. Besides, a significant difference in serum MIF level was observed in BC cases with progesterone receptor (PR) negativity compared to those with PR positivity ( P = 0.046). Moreover, a significant association was depicted between the rs1049829 variant of MIF gene and the protective effect against BC meanwhile the rs755622 variant demonstrated no significant link with BC risk. Conclusions This study revealed that serum MIF levels may be regarded as a promising serum tumor marker for BC. Also, the rs1049829 variant of the MIF gene is considered a protective candidate against BC. Graphical Abstract
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