Open AccessInteraction between cyclooxygenase-2 and insulin-like growth factor in breast cancer: A new field for prevention and treatment
Author(s) -
Giuliana Cássia Morrone Taromaru,
Vilmar Marques de Oliveira,
Maria Antonieta Longo Galvão Silva,
Wagner Ricardo Montor,
Fábio Bagnoli,
José Francisco Rinaldi,
Tsutomu Aoki
Publication year - 2011
Publication title -
oncology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.766
H-Index - 54
eISSN - 1792-1082
pISSN - 1792-1074
DOI - 10.3892/ol.2011.532
Subject(s) - ductal carcinoma , tissue microarray , oncogene , breast cancer , medicine , cancer , molecular medicine , ki 67 , carcinogenesis , oncology , cyclooxygenase , immunohistochemistry , cell cycle , insulin like growth factor , growth factor , cancer research , biology , receptor , enzyme , biochemistry
The objective of this study was to evaluate the correlation between cyclooxygenase-2 (COX-2) and markers of cell proliferation and apoptosis, including, Bcl-2, Bax, Ki-67 and the type I insulin-like growth factor (IGF) receptor (IGF1-R) in ductal carcinoma in situ (DCIS) and infiltrating ductal carcinoma (IDC), present in the same surgical specimen. A total of 110 cases were evaluated using tissue microarrays. Cases were classified in scores from 0 to 3 according to pre-defined methods. The results showed that the positivity rates were COX-2 in 87% of cases in DCIS and IDC; Bcl-2 in 55% of cases in DCIS and IDC; Bax in 23% of cases in IDC and 19% in DCIS, IGF-1 in 24% of cases in DCIS and IDC; and Ki-67 in 81% of cases in DCIS and IDC. We also observed a positive correlation between the expression of COX-2 and IGF1-R (p=0.045). Our results demonstrate a positive correlation between the expression of COX-2 and IGF1-R in DCIS and IDC, demonstrating that they are involved in breast cancer carcinogenesis. Further studies are required to prove the effectiveness of COX-2 and IGF1-R inhibitors for the prevention and treatment of breast cancer, as well as to explain their mechanism of action.