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

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.

Dipotassium Glycyrrhizininate Improves Skin Wound Healing by Modulating Inflammatory Process

“…In response to tissue injury, several pro-inflammatory factors are synthesized and secreted by neutrophils, macrophages, and other cells, as well as anti-inflammatory mediators and growth and structural factors, which act in the different phases of wound healing [ 45 ]. At first, platelets, leucocytes, and endothelial cells release inflammatory mediators, mainly COX-2 [ 48 , 49 ], IL-1 e IL-8 [ 11 , 50 , 51 ], TNF-α, IFN-γ, CXCL1, CXCL8 [ 52 , 53 ], and adhesion molecules [ 6 , 7 ]. These mediators and others recruit large numbers of inflammatory cells [ 54 , 55 , 56 ], mainly neutrophils [ 52 , 53 ], to the wound site, which aim to degrade the damaged matrix and remove the damaging agent, preventing infection [ 53 , 57 ].…”

Genetic predisposition to early mycosis fungoides: investigating genetic polymorphisms in tissue-resident memory T-cell genes

“…In addition, several studies have noted the role of polymorphisms in genes related to inflammation and lymphocyte activation, such as COX2, IL2, IL13, IL17, STAT3, miRNAs, CTLA4, TGFB1, and VDR. [26][27][28][29][30][31][32][33][34] However, other studies have discounted any association between MF and CTLA4, TGFB1, or VDR. [35][36][37][38] Similarly, our findings did not support any influence of CTLA4 on MF.…”

Cyclooxygenase-2 Gene Polymorphisms – 765G&#x3e;C and –1195A&#x3e;G and Mycosis Fungoides

“…We read the publication on “Cyclooxygenase-2 (COX-2) gene polymorphisms –765G>C and –1195A>G and mycosis fungoides risk” with a great interest. Sayed et al [1] found that “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[1]. ” We would like to share ideas on this finding.…”