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Elevated expression of cyclooxygenase‐2 in breast cancer and ductal carcinoma in situ has no correlation with established prognostic markers
Author(s) -
Singh Ranger Gurpreet,
Jewell Andrew,
Thomas Valerie,
Mokbel Kefah
Publication year - 2004
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/jso.20142
Subject(s) - medicine , ductal carcinoma , breast cancer , proportional hazards model , immunohistochemistry , cancer , pathology , oncology , clinical significance , carcinoma in situ
Background and Objectives Elevated expression of cyclooxygenase‐2 (COX‐2) has been established to be a feature of breast cancer. There has been inconsistency in the literature regarding the precise significance of this—some studies have found no clinicopathological relevance at all, whilst others have concluded COX‐2 expression is an important biomarker in invasive disease and pre‐cancerous lesions, correlating with poor prognostic features. We studied COX‐2 expression in invasive ductal cancer (IDC) specimens and ductal carcinoma in situ (DCIS) in order to clarify these issues. Method Archival specimens of IDC and DCIS (n = 39) were stained with a polyclonal antibody to COX‐2. Results were correlated with recognised clinicopathological parameters. Results COX‐2 expression occurred in 36.7% of IDCs and 54.5% of DCIS lesions. There was no correlation between increased expression and any clinicopathological features. COX‐2 expression did not occur in adjacent non‐cancerous tissue (ANCT). Conclusion We have confirmed that COX‐2 expression does occur in invasive cancers, in DCIS, and is not associated with established prognostic markers. The presence of COX‐2 expression in DCIS and invasive cancers has positive implications for the future prevention and treatment of breast cancer with COX‐2 inhibitors. A large proportion of tumours are, however, COX‐2 negative and may be poor candidates for COX‐2 suppression. J. Surg. Oncol. 2004;88:100–103. © 2004 Wiley‐Liss, Inc.