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BMC Cancer  2006 

Cyclo-oxygenase-2 (Cox-2) expression and resistance to platinum versus platinum/paclitaxel containing chemotherapy in advanced ovarian cancer

DOI: 10.1186/1471-2407-6-182

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Abstract:

A retrospective study was performed to investigate the association of COX-2 with outcome and response to platinum versus platinum/paclitaxel in 68 primary ovarian cancer. COX-2 immunoreaction was performed on paraffin-embedded sections by using rabbit polyclonal antiserum against COX-2.In the overall series, COX-2 positivity was found in a statistically significant higher percentage of not responding cases than in patients responding to chemotherapy (n = 15/21; 71.4% versus n = 17/47; 36.1%; p value = 0.0072). A higher percentage of COX-2 positivity was found in patients unresponsive (n = 11/13; 84.6%) versus patients responsive to platinum-based chemotherapy (n = 9/26; 34.6%). In cases administered platinum/paclitaxel, COX-2 positivity was found in 4 out of 8 (50%) of un responsive versus 8 out of 21 (38.1%) of responsive cases. Logistic regression analysis of parameters likely to affect response to treatment resulted in a p value = 0.17 for the interaction COX-2/type of treatment.Although these findings need to be confirmed in a larger series, our study suggests a possible indication that there is a difference in the influence of COX-2 on response depending on treatment regimen.Ovarian cancer represents the fifth leading cause of death for cancer in women [1]. More than 70% of cases present with advanced stage of disease at diagnosis and despite advances in cytoreductive surgery and establishment of carboplatin/paclitaxel combination as the standard chemotherapy regimen, intrinsic or acquired tumor chemoresistance remains the major determinant of chemotherapy failure and unfavourable clinical outcome [1,2].Several molecular alterations have been proposed to support tumor resistance to cytotoxic drugs, such as the expression of MDR phenotype, mutation of p53, bcl2 overexpression [3-5], but only very recently it has been recognized that specific molecular or biological profiles might characterize tumor sensitivity to classes of agents with different mechanisms of ac

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