method used to predict the likelihood of success to anti-estrogen therapy in breast carcinoma. ER-positive breast carcinomas are likely to respond to various endocrine treatments, causing the monitoring of ER activity an essential variable in disease and treatment progression. In 2002, 6 cases of breast carcinoma were received, characterized, and analyzed through the ERT IHC assessment. The level of known ER activity was classified (negative, low, medium, and high) and selected for observation. After embedment in a paraffin block, the samples were stained using a hematoxylin and eosin staining (H & E staining) system. The IHC analysis was then performed the same day using anti-ER monoclonal antibodies, and resulted in a consistently strong correlation in the carcinoma samples with ER activity, whereas the level of ER activity increased, the IHC response increased respectively. Various target antibodies may be used in the IHC assessment of the ER. Typically, the antibody used for this experiment is the anti-estrogen Receptor (ER) (SP1) Rabbit Monoclonal Antibody. Employing SP1 allows for the detection of estrogen receptor (ER) antigens in sections of the fixed patient samples. In junction with light microscopy, the approximate ER activity can be estimated using the level of staining of the cell's components. The anti-ER (SP1) antibody targets the ER alpha protein (ERα) located in the nucleus of ER-positive normal and neoplastic cells. The anti-ER (SP1) antibody's response is a useful indication of the progression, management, and prediction of therapy outcome of breast cancer. These antibodies are commercially available from 3 commonly used auto strain vendors- Dako, Leica, and Ventana, and in a study by Kornaga et al, all behaved similarly in the semi-quantitative analysis of breast cancer biopsy samples. Estrogen receptor pathway Estrogen receptor pathway schematic The schematic below models the activity pathway of the estrogen receptor. In the typical estrogen pathway (i) estrogen or other selective estrogen receptor modulators (SERMs) are bound to the estrogen receptor (ER) via the coregulatory proteins (CoReg) in the nucleus. Alternately, the estrogen or SERM complexes may occur through the ER located adjacent to the plasma membrane (ii) with the help of adaptor proteins such as caveolin 1 or SHC1, which target the ER complexes to the plasma membrane. Activation of the ER complex causes increased kinase activity in phosphoinositide 3-kinases (PI3K) and mitogen-activated protein kinase (MAPK) as well as increases in concentrations of signaling molecules like calcium and nitric oxide. Estrogen receptor test and