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环氧化酶-2 基因多态性 -765G>C 和 -1195A>G 与蕈样肉芽肿风险的关系。

Cyclooxygenase-2 Gene Polymorphisms -765G>C and -1195A>G and Mycosis Fungoides Risk.

机构信息

Department of Dermatology, Faculty of Medicine, Cairo University, Giza, Egypt.

Department of Dermatology and Venereology, National Research Centre, Giza, Egypt.

出版信息

Dermatology. 2021;237(1):17-21. doi: 10.1159/000504840. Epub 2019 Dec 17.

Abstract

BACKGROUND

Cyclooxygenase-2 (COX-2) is an inducible modulator of inflammation that acts through increasing prostaglandin levels and has been described as a major mediator linking inflammation to cancer. Previous studies supported that COX-2-765G>C and -1195A>G polymorphisms were associated with increased risk of several solid tissue cancers as well as some hematological malignancies.

OBJECTIVE

The aim of the study was to elucidate the association between functional COX-2 genotypes (-765G>C and -1195A>G) polymorphisms and the risk of developing mycosis fungoides (MF).

METHODS

This was a hospital-based, case-control study of 70 MF patients and 100 MF-free controls. We genotyped COX-2 -1195A>G, -765G>C, and -8473T>C polymorphisms by using the PCR-restriction fragment length polymorphism method.

RESULTS

The AA genotype in the COX-2 -1195A>G gene polymorphism and the GC genotype in the COX-2 -765G>C gene were significantly more frequent among MF patients compared to controls (p< 0.001 and p = 0.002, respectively).

CONCLUSION

The -results indicate a possible role of COX-2 genes in the pathogenesis of MF. These novel findings may allow for notable future advances, as it will enable the identification of the -individuals most susceptible to MF.

摘要

背景

环氧化酶-2(COX-2)是一种炎症的诱导调节剂,通过增加前列腺素水平起作用,并被描述为将炎症与癌症联系起来的主要介质。先前的研究支持 COX-2-765G>C 和-1195A>G 多态性与几种实体组织癌症以及一些血液恶性肿瘤的风险增加有关。

目的

本研究旨在阐明功能性 COX-2 基因型(-765G>C 和-1195A>G)多态性与蕈样肉芽肿(MF)发病风险之间的关系。

方法

这是一项基于医院的病例对照研究,共纳入 70 例 MF 患者和 100 例 MF 对照组。我们采用 PCR-限制性片段长度多态性方法检测 COX-2-1195A>G、-765G>C 和-8473T>C 多态性。

结果

与对照组相比,MF 患者中 COX-2-1195A>G 基因多态性的 AA 基因型和 COX-2-765G>C 基因的 GC 基因型更为常见(p<0.001 和 p=0.002)。

结论

结果表明 COX-2 基因可能在 MF 的发病机制中起作用。这些新发现可能会带来显著的未来进展,因为它将能够识别最易患 MF 的个体。

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