Laga AC, Zander DS, Cagle PTPrognostic significance of cyclooxygenase 2 expression in 259 cases of non-small cell lung cancer. Arch Pathol Lab Med 129: 1113-1117

Department of Pathology, Baylor College of Medicine, Houston, TX, USA.
Archives of pathology & laboratory medicine (Impact Factor: 2.84). 10/2005; 129(9):1113-7. DOI: 10.1043/1543-2165(2005)129[1113:PSOCEI]2.0.CO;2
Source: PubMed


Previous studies report that increased expression of cyclooxygenase 2 (COX-2) correlates with poor clinical outcome in several malignancies, including non- small cell lung carcinoma (NSCLC). Cyclooxygenase 2 inhibitors have been reported to effectively inhibit carcinogenesis in colon cancer experimental models.
We examined COX-2 expression in 259 cases of NSCLC to evaluate its prognostic significance.
Sections of NSCLC from patients with a median 5-year follow-up were immunostained with COX-2 monoclonal antibody (1:150) using the Dako mouse EnVision;pl system. Extent of COX-2 expression in neoplastic cells was recorded as follows: 0, 0% to 10% of cells positive; 1, 11% to 33% positive; 2, 34% to 66% positive; and 3, more than 66% positive. Intensity was scored as either increased (+) or not increased (-), compared to internal control smooth muscle and endothelial cells. Kaplan-Meier analysis was used to assess the relationship between survival and COX-2 expression, using the log-rank test for statistical significance.
No relationship was found between the extent and/or the intensity of COX-2 expression and patient survival when the entire cohort was considered. However, when separately analyzed according to disease stage and intensity of COX-2 expression, a significant relationship (P = .03) between increased COX-2 expression and shortened patient survival was found only in patients with stage I and II NSCLC.
To our knowledge, this is the largest series of NSCLCs in which COX-2 has been investigated as a prognostic marker. The findings in this large series support previous studies of smaller cohorts that reported that increased COX-2 expression predicts poor outcome in patients with early-stage NSCLC.

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    • "Our result is concordant with previous literature demonstrating the over-expression of COX-2 (Murata H et al. 1999) (Fig. 1b, 5a). Our results demonstrate that the expression of COX-2 increase with advancement of tumor stage which is also concordant with previous report (Khunamornpong et al. 2009; Laga et al. 2005) (Fig. 1b, 5a). H. pylori infection is one of the important factors for the Gastric Carcinoma. "

    International Journal of Advanced Research 02/2014;
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    • "Although COX-2 expression was also found higher in female patients, patients with ages≤60 years, non-smokers, moderate and well differentiated tumors, nodal metastasis, and in stages III-IV, the difference had no statistical significance. Studies examining the relationship between COX-2 tumor expression and survival among lung cancer patients were inconsistent, with reports of an inverse relationship with survival [35], no association [36], or a direct association with survival [37]. In our study, there was no correlation between COX-2 expression and patient's overall survival. "
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    ABSTRACT: To evaluate the expression of EGFR and COX-2 and their correlation with prognosis in NSCLC METHODS: The paraffin embedded tumor samples of 50 NSCLC patients receiving radical resection were analyzed immunohistochemically for EGFR and COX-2 expression and their prognostic values were explored. The positive rate of EGFR protein in NSCLC tumor cells was 46%, which was significantly higher than its expression in normal lung (p = 0.0234) and paracancerous tissues (p = 0.020). EGFR expression was significantly higher in nodal positive than in nodal negative patients (p = 0.04). The mean survival time for EGFR positive patients (31 months) was significantly lower than that for patients with EGFR negative expression (48 months) (p = 0.008,). In patients receiving post-operation thoracic irradiation, the mean survival time for EGFR positive patients was significantly lower than that for patients without EGFR positive expression (25 vs. 48 months, P = 0.004). The positive rate of COX-2 protein expression in NSCLC tumor cells was 90%, which was significantly higher than that in normal tissue(p = 0.00) and paracancerous tissue (p = 0.00). There was no correlation between COX-2 expression and patient survival, and no correlation between COX-2 and EGFR protein expression (P = 0.555). COX-2 and EGFR are over-expressed in NSCLC. EGFR is an independent prognostic factor and a predictive factor for radiotherapy response in NSCLC.
    Journal of Experimental & Clinical Cancer Research 03/2011; 30(1):27. DOI:10.1186/1756-9966-30-27 · 4.43 Impact Factor
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    • " 2008 – IOS Press and the authors. All rights reserved COX-2 levels in NSCLC and their importance in lung carcinogenesis [12] [13] [14]. Over-expression of COX-2 has been proposed as a biomarker for biologically aggressive types of NSCLC and poorer survival [15] [16] [17]. "
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    ABSTRACT: We evaluated the occurrence of mutations in P53, K-RAS, COX-2, expression of COX-2 and hTERT and relations among clinicopathological signs. P53 mutations were identified in 34.4% of tumours, the majority of them occurring in SCC (squamous cell carcinoma, 55.6%). K-RAS was mutated in 12.2% of NSCLC tumours, the majority of the mutations being found in ADC (adenocarcinoma, 27.0%). Mutational screening detected three different COX-2 mutations and five different P53 mutations, published for the first time. With RT-PCR we observed that the expression of the tested genes, hTERT and COX-2, was highly significant for ADC (p < 0.01) and SCC (p < 0.05). Statistical analysis of the combined results revealed significant correlation between expression of COX-2 and hTERT (p < 0.001), hTERT expression and staging (p < 0.05) and survival (p < 0.01). A positive correlation between COX-2 expression and K-RAS mutation (p <0.05) was also observed. This study provides insight into associations between the analysed biomarkers and the clinical-pathological data of the patients.
    Disease markers 10/2008; 25(2):97-106. DOI:10.1155/2008/232743 · 1.56 Impact Factor
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