Ressure device (Colin BP-8800; Colin Corporation, Hayashi, Japan) after the subject had rested for five minutes. We used the definition of MetS as proposed by the American Heart Association and the National Heart, Lung, and Blood Institute [21]. These criteria require at least three of the following components: abdominal obesity, triglycerides 150 mg/dl or receiving drug treatment, HDL cholesterol
Provide blood samples at the National Cancer Center Hospital, Korea, between April 2001 and December 2004. Among a total of 856 cases considered for the initial recruitment, 747 patients remained eligible after exclusion for the following: (1) distant metastasis at diagnosis (8 cases), (2) ductal carcinoma in situ (70 cases), (3) cancer with unreported ER/PR status (29 cases), (4) male gender (1 c
Of DC-SCRIPT are associated with reduced tumor aggressiveness. The association is particularly strong for small tumors with high ESR1 or low ESR2 mRNA levels or both. Finally, although DC-SCRIPT negatively regulates ESR1 and PGR activity, DC-SCRIPT levels measured in theSieuwerts et al. Breast Cancer Research 2010, 12:R103 http://breast-cancer-research.com/content/12/6/RPage 9 ofprimary tumors are
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
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
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
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