Either ESR1-positive and/or ESR2-low pT1 tumors.Introduction Estrogens influence the aggressiveness of breast cancer through their cognate nuclear receptors. In particular, the estrogen receptor-alpha (ERa) (ESR1) - present in tumor cells of about 70 to 75 of all breast tumors is considered crucial because of its proliferationinducing actions and for that reason is an important target for therap
Either ESR1-positive and/or ESR2-low pT1 tumors.Introduction Estrogens influence the aggressiveness of breast cancer through their cognate nuclear receptors. In particular, the estrogen receptor-alpha (ERa) (ESR1) - present in tumor cells of about 70 to 75 of all breast tumors is considered crucial because of its proliferationinducing actions and for that reason is an important target for therap
Tcome are listed in Table 1.RNA isolation and quantitative RT-PCRThe protocol to study biological markers associated with disease outcome was approved by the medical ethics committee of the Erasmus Medical Center (Rotterdam, The Netherlands) (MEC 02.953). This retrospective study used 1,505 M0 (no metastasis) and 32 M1 (with metastasis) blind-coded freshly frozen primary tumor tissues of female pa
Ity Nijmegen Medical Centre, Geert Grooteplein 28, Nijmegen, 6525 GA, The Netherlands Full list of author information is available at the end of the articleof breast cancers. Apart from breast epithelial tumor cells, ESR2 is also expressed in adjacent infiltrating lymphocytes, fibroblasts, and endothelial cells, all of which are known to influence tumor growth [3]. However, its precise role in bre
Either ESR1-positive and/or ESR2-low pT1 tumors.Introduction Estrogens influence the aggressiveness of breast cancer through their cognate nuclear receptors. In particular, the estrogen receptor-alpha (ERa) (ESR1) - present in tumor cells of about 70 to 75 of all breast tumors is considered crucial because of its proliferationinducing actions and for that reason is an important target for therap
Tivities of ESR1 and progesterone receptor (PGR) [7]. We also showed that DC-SCRIPT was an independent prognostic factor, particularly for hormone receptor-positive breast cancer. This led us to postulate that the anti-proliferative effect of DC-SCRIPT in breast cancer cells could be mediated by simultaneous modulation of the activity of multiple nuclear receptors. To provide a higher level of evi
Tivities of ESR1 and progesterone receptor (PGR) [7]. We also showed that DC-SCRIPT was an independent prognostic factor, particularly for hormone receptor-positive breast cancer. This led us to postulate that the anti-proliferative effect of DC-SCRIPT in breast cancer cells could be mediated by simultaneous modulation of the activity of multiple nuclear receptors. To provide a higher level of evi
R JS, Kietz S, Wimalasena J, Gustafsson JA: Estrogen receptor beta inhibits 17beta-estradiol-stimulated proliferation of the breast cancer cell line T47D. Proc Natl Acad Sci USA 2004, 101:1566-1571. 2. Liu MM, Albanese C, Anderson CM, Hilty K, Webb P, Uht RM, Price RH Jr, Pestell RG, Kushner PJ: Opposing action of estrogen receptors alpha and beta on cyclin D1 gene expression. J Biol Chem 2002, 27