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Title: Correlative expression of cyclooxygenase-1 (Cox-1) and human epidermal growth factor receptor type-2 (Her-2) in endometrial cancer. Author: Sugimoto T, Koizumi T, Sudo T, Yamaguchi S, Kojima A, Kumagai S, Nishimura R. Journal: Kobe J Med Sci; 2007; 53(5):177-87. PubMed ID: 18204294. Abstract: OBJECTIVES: Cyclooxygenase-2 (Cox-2) is known to be associated with tumorigenesis in many cancers including endometrial cancer, while there is substantial evidence for the tumorigenicity of cyclooxygenase-1 (Cox-1). However, little is known about the involvement of Cox-1 in the development of endometrial cancer. The aim of this study was to determine whether cyclooxygenase-1 or -2 (Cox-1, Cox-2) is tumorigenetic, as well as whether these two cyclooxygenase isoforms correlate with the clinicopathological characteristics or with another two biomarkers, human epidermal growth factor receptor type-2 (Her-2) and vascular endothelial growth factor (VEGF), of endometrial cancer. METHODS: At first, Cox-1 and Cox-2 levels in eight endometrial cancer cell lines were determined by means of real-time PCR. At second, the levels of four biomarkers (Cox-1, Cox-2, Her-2, and VEGF) in 70 endometrial cancer samples were determined by means of real-time PCR. Pairs of these biomarkers were subjected to correlation as each biomarker and clinical status or survival. RESULTS: In the eight cell lines, the expression of Cox-1 and Cox-2 showed major variations in their mRNA levels. Analysis of the patient samples showed that the mRNA expression of Cox-1 was elevated significantly in the G1 (P=0.021) and G2 (P=0.036) groups, as was the mRNA expression of Her-2 in the two groups (P=0.036 and P=0.0029, respectively). The mRNA expression of Cox-1 and Her-2 were correlated (CI=0.671). None of the three biomarkers, Cox-1, Cox-2, and Her-2, was correlated with clinical status such as FIGO classification, myometrial invasion, or clinical outcome. CONCLUSION: Cox-1, together with Her-2, may be involved in the early stage of endometrial cancer development.[Abstract] [Full Text] [Related] [New Search]