Taromaru Giuliana Cássia Morrone, DE Oliveira Vilmar Marques, Silva Maria Antonieta Longo Galvão, Montor Wagner Ricardo, Bagnoli Fabio, Rinaldi José Francisco, Aoki Tsutomu
Department of Obstetrics and Gynecology, Irmandade da Santa Casa de Misericórdia de São Paulo and Santa Casa de São Paulo, Faculty of Medical Sciences, São Paulo, Brazil.
Oncol Lett. 2012 Mar;3(3):682-688. doi: 10.3892/ol.2011.532. Epub 2011 Dec 21.
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.
本研究的目的是评估同一手术标本中导管原位癌(DCIS)和浸润性导管癌(IDC)中环氧化酶-2(COX-2)与细胞增殖和凋亡标志物之间的相关性,这些标志物包括Bcl-2、Bax、Ki-67和I型胰岛素样生长因子(IGF)受体(IGF1-R)。使用组织微阵列对总共110例病例进行了评估。根据预定义方法将病例分为0至3分。结果显示,DCIS和IDC中COX-2的阳性率为87%;DCIS和IDC中Bcl-2的阳性率为55%;IDC中Bax的阳性率为23%,DCIS中为19%;DCIS和IDC中IGF-1的阳性率为24%;DCIS和IDC中Ki-67的阳性率为81%。我们还观察到COX-2与IGF1-R的表达之间存在正相关(p=0.045)。我们的结果表明,DCIS和IDC中COX-2与IGF1-R的表达之间存在正相关,表明它们参与了乳腺癌的致癌过程。需要进一步研究以证明COX-2和IGF1-R抑制剂对乳腺癌预防和治疗的有效性,并解释其作用机制。