Premium
COX‐2 expression in DCIS: correlation with VEGF, HER‐2/ neu , prognostic molecular markers and clinicopathological features
Author(s) -
Perrone G,
Santini D,
Vincenzi B,
Zagami M,
La Cesa A,
Bianchi A,
Altomare V,
Primavera A,
Battista C,
Vetrani A,
Tonini G,
Rabitti C
Publication year - 2005
Publication title -
histopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.626
H-Index - 124
eISSN - 1365-2559
pISSN - 0309-0167
DOI - 10.1111/j.1365-2559.2005.02132.x
Subject(s) - immunohistochemistry , breast cancer , pathology , vascular endothelial growth factor , medicine , proportional hazards model , ductal carcinoma , mammary gland , cancer , progesterone receptor , vegf receptors , oncology , estrogen receptor
Aims : There is considerable evidence that links COX‐2 to the development of cancer. The aim of our study was to assess, by immunohistochemistry, COX‐2 expression in ductal carcinoma in situ (DCIS) and its possible correlation with HER‐2/ neu , vascular endothelial growth factor (VEGF) expression and other common immunohistochemical parameters (p53, ER, PGR, Ki67). Methods and results : Tissue samples of 49 archival cases of DCIS without any invasive component were analysed for COX‐2, HER‐2/ neu , VEGF, oestrogen and progesterone receptors, Ki67 and p53 by immunohistochemistry using specific antibodies. COX‐2 expression was detected in 43 (87.8%) tissue samples, of which 12 (24.5%) were graded as weak, 22 (44.9%) as moderate and nine (8.4%) as high expression. Only six (12.2%) lesions were negative for COX‐2 expression. VEGF expression was detected in 93.8% of samples; 66.7% of lesions were found to be positive for HER‐2/ neu expression. Furthermore, COX‐2 expression was significantly correlated with VEGF expression ( P = 0.003). A significant positive correlation was also observed between COX‐2 and HER‐2/ neu expression ( P < 0.0001). Conclusions : Our results suggest that COX‐2 is highly expressed in DCIS and takes part in the molecular pathway implicated in progression of breast cancer and may provide a rationale for targeting COX‐2 in preinvasive breast cancer therapy.