Prognostic Significance of Cyclooxygenase-2(COX-2) Expression in Primary, Resected Non-Small Cell Lung Cancer

2004 ◽  
Vol 56 (2) ◽  
pp. 169
Author(s):  
Hak Ryul Kim ◽  
Sei Hoon Yang ◽  
Eun Taik Jeong
Lung Cancer ◽  
2003 ◽  
Vol 41 ◽  
pp. S182 ◽  
Author(s):  
Iidiko Csiki ◽  
Adriana Gonzalez ◽  
David P. Carbone ◽  
Shiva Gautam ◽  
Alan Sandler ◽  
...  

2002 ◽  
Vol 235 (3) ◽  
pp. 440-443 ◽  
Author(s):  
Jan Brabender ◽  
JiMin Park ◽  
Ralf Metzger ◽  
Paul M. Schneider ◽  
Reginald V. Lord ◽  
...  

Haigan ◽  
2006 ◽  
Vol 46 (6) ◽  
pp. 705-710
Author(s):  
Yoshimasa Tanikawa ◽  
Hiroyuki Taniguchi ◽  
Osamu Nishiyama ◽  
Masahiro Aoyama ◽  
Yoshitaka Hibino ◽  
...  

2011 ◽  
Vol 29 (32) ◽  
pp. 4320-4326 ◽  
Author(s):  
Harry J.M. Groen ◽  
Hannie Sietsma ◽  
Andrew Vincent ◽  
Monique M.H. Hochstenbag ◽  
John W.G. van Putten ◽  
...  

Purpose Cyclooxygenase-2 (COX-2) protein expression in patients with non–small-cell lung cancer (NSCLC) may be not only a prognostic marker but also predictive for COX-2 inhibition. We hypothesized that COX-2 expression is associated with shorter survival and that celecoxib, being a potent COX-2 inhibitor, increases tumor response and survival. Patients and Methods A phase III study was performed in patients with stage IIIb/IV NSCLC who had pathologic confirmation, no prior chemotherapy, Eastern Cooperative Oncology Group performance status of 0 to 2, and adequate organ function. Treatment consisted of docetaxel and carboplatin every 3 weeks for five cycles. Patients were randomly assigned to receive celecoxib 400 mg or placebo twice daily. COX-2 expression on tumor cells was detected by immunohistochemistry. Primary end point was overall survival (OS). Results From July 2003 to December 2007, 561 patients were randomly assigned. Toxicity was mild, and no increase in cardiovascular events was observed. Tumor response was 38% in the celecoxib arm and 30% in the placebo arm (P = .08). Median progression-free survival was 4.5 months (95% CI, 4.0 to 4.8) for the celecoxib arm and 4.0 months (95% CI, 3.6 to 4.9) for the placebo arm (hazard ratio [HR], 0.8; 95% CI, 0.6 to 1.1; P = .25). Median OS was 8.2 months (95% CI, 7.5 to 8.8) for both treatment arms (HR, 0.9; 95% CI, 0.6 to 1.2; P = .32). COX-2 expression did not independently predict survival. Benefit from celecoxib, restricted to patients with low COX-2 expression, was not significant when adjusted for prognostic factors. Conclusion In advanced NSCLC, celecoxib does not improve survival. In this study, COX-2 expression was not a prognostic biomarker and had no predictive value when celecoxib was added to chemotherapy.


2012 ◽  
Vol 30 (16) ◽  
pp. 2019-2020 ◽  
Author(s):  
Martin J. Edelman ◽  
Lydia Hodgson ◽  
Xiaofei Wang ◽  
Robert A. Kratzke ◽  
Everett E. Vokes

2017 ◽  
Vol 35 (19) ◽  
pp. 2184-2192 ◽  
Author(s):  
Martin J. Edelman ◽  
Xiaofei Wang ◽  
Lydia Hodgson ◽  
Richard T. Cheney ◽  
Maria Q. Baggstrom ◽  
...  

Purpose Tumor overexpression of cyclooxygenase-2 (COX-2) has been associated with worse outcome in non–small-cell lung cancer (NSCLC). In Cancer and Leukemia Group B (CALGB) 30203, we found that the selective COX-2 inhibitor celecoxib in addition to chemotherapy in advanced NSCLC improved progression-free and overall survival in patients with moderate to high COX-2 expression by immunohistochemistry (IHC). CALGB 30801 (Alliance) was designed to prospectively confirm that finding. Patients and Methods Patients with NSCLC (stage IIIB with pleural effusion or stage IV according to American Joint Committee on Cancer [sixth edition] criteria) were preregistered, and biopsy specimens were analyzed for COX-2 by IHC. Patients with COX-2 expression ≥ 2, performance status of 0 to 2, and normal organ function were eligible. Chemotherapy was determined by histology: carboplatin plus pemetrexed for nonsquamous NSCLC and carboplatin plus gemcitabine for squamous histology. Patients were randomly assigned to celecoxib (400 mg twice per day; arm A) or placebo (arm B). The primary objective was to demonstrate improvement in progression-free survival in patients with COX-2 index ≥ 4 with hazard ratio of 0.645 with approximately 85% power at two-sided significance level of .05. Results The study was halted for futility after 312 of the planned 322 patients with COX-2 index ≥ 2 were randomly assigned. There were no significant differences between the groups (hazard ratio, 1.046 for COX-2 ≥ 4). Subset analyses evaluating histology, chemotherapy regimen, and incremental COX-2 expression did not demonstrate any advantage for COX-2 inhibition. Elevation of baseline urinary metabolite of prostaglandin E2, indicating activation of the COX-2 pathway, was a negative prognostic factor. Values above the third quartile may have been a predictive factor. Conclusion COX-2 expression by IHC failed to select patients who could benefit from selective COX-2 inhibition. Urinary metabolite of prostaglandin E2 may be able to identify patients who could benefit from COX-2 inhibition.


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