Abstract
Cyclooxygenase-2 (COX-2) and human epidermal growth factor receptor type 2 (HER-2) are associated with tumorigenesis. Studies have shown that HER-2 can regulate COX-2 expression. The aim of this study was to evaluate the correlation between COX-2 and HER-2 expression in normal breast epithelium and in ductal carcinoma in situ (DCIS) and invasive ductal carcinoma (IDC) present in the same breast. Cross-sectional study at the Mastology Unit of the Department of Gynecology and Obstetrics, Santa Casa de Misericórdia de São Paulo Hospital. COX-2 and HER-2 were detected using immunohistochemistry on 100 tissue fragments. HER-2 > +2 was subjected to fluorescence in situ hybridization (FISH). COX-2 expression was detected in 87%, 85% and 75% of IDC, DCIS and normal epithelium, respectively. HER-2 expression was detected in 34% of IDC and 34% of DCIS. COX-2 in DCIS correlated with HER-2 in IDC (P = 0.049) and DCIS (P = 0.049). COX-2 in normal epithelium correlated with HER-2 in IDC (P = 0.046) and DCIS (P = 0.046). COX-2 in IDC was not associated with HER-2 (P = 0.235). Comparison between COX-2 and HER-2 in DCIS showed that there was a statistically significant difference with regard to nuclear grades II and III and presence of comedonecrosis (P < 0.001). In IDC, there was significant expression with nuclear grades II and III and histological grade II (P < 0.001). Our findings provide evidence that HER-2 and COX-2 regulate each other.
Highlights
Prostaglandins are known to participate in multiple physiological and pathological processes, including wound healing, cardiovascular disease, inflammation and the development and growth of malignant tumors.[1]
The aim of this study was to evaluate the correlation between COX-2 and human epidermal growth factor receptor type 2 (HER-2) expression in ductal carcinoma in situ (DCIS) and invasive ductal carcinoma (IDC) from the same breast as well as in normal epithelium
COX-2 was positively detected at frequencies of 87%, 85% and 75% in IDC, DCIS and normal epithelium respectively
Summary
Prostaglandins are known to participate in multiple physiological and pathological processes, including wound healing, cardiovascular disease, inflammation and the development and growth of malignant tumors.[1]. COX-2 expression is induced by pro-inflammatory cytokines, tumor promoters, growth factors and viral transformation.[9,10] How COX-2 overexpression results in tumorigenesis and how COX-2 selective agents mediate chemopreventive effects are issues that still need further clarification Another important protein, closely related to breast cancer, is human epidermal growth factor receptor type 2 (HER-2), one of the four receptors belonging to the HER family.[11,12] This receptor presents proliferation-stimulating responses upon ligand binding.[13]. HER-2 overexpression often results from increased c-erb-b2 gene activation.[14,15] Its overexpression becomes more important when this protein forms heterodimers with other HER family receptors, such as human epidermal growth factor receptor type 3 (HER-3) This leads to hyperactive cell signaling pathways and the emergence of a situation of uncontrolled cell proliferation, culminating in tumorigenesis.[16]. Many studies have already analyzed HER-2 and COX-2 expression in ductal carcinoma in situ and invasive ductal carcinoma, but most of these studies were carried out on samples from different women, thereby restricting the usefulness of these data for studying tumor progression
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
