AI Article Synopsis

  • The study aimed to evaluate the expression of cyclooxygenase-2 (Cox-2) in breast carcinomas to assess its clinical significance.
  • Analysis of 600 samples revealed that higher Cox-2 expression was linked to advanced tumor stages, Her-2/neu amplification, and aggressive tumor characteristics.
  • Despite these associations, the study did not find a significant link between Cox-2 levels and overall or disease-free survival, suggesting Cox-2 could serve as a prognostic marker and potential therapeutic target.

Article Abstract

Purpose: The objective of this study was to evaluate breast carcinomas for the expression of cyclooxygenase-2 (Cox-2) using a tissue microarray (TMA) and to determine its clinical and prognostic relevance.

Methods: We analyzed Cox-2 expression in 600 samples from 200 breast carcinomas immunohistochemically performing TMA technology and semiquantitative analysis. Results were correlated with various clinicopathological variables and follow-up data. Expression of estrogen receptor, progesterone receptor, Ki-67, and Her-2/neu-oncogene was analyzed and correlated with Cox-2 status.

Results: We observed a moderate or strong cytoplasmic staining for Cox-2 in 78 (40.6%) of breast carcinomas. Increased Cox-2 expression corresponded to higher pT stage ( P=0.038), amplification of Her-2/neu ( P=0.032), lymphovascular invasion ( P=0.006), a high MIB-1 labeling index (LI) ( P<0.001), and histological grading ( P=0.013). We also observed an inverse relationship between strong Cox-2 expression and estrogen and progesterone receptor content of tumors ( P=0.037 and P=0.010). However, we could not demonstrate a significant association between Cox-2 staining and overall survival or disease free survival time.

Conclusions: These results suggest that Cox-2 expression is significantly associated with less differentiated and more aggressive breast carcinomas and might therefore be a useful prognostic indicator as well as a target for therapy.

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Source
http://dx.doi.org/10.1007/s00432-003-0459-1DOI Listing

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