Disease relevance of Carcinoma, Ductal, Breast

• p53 mutations in mammary ductal carcinoma in situ but not in epithelial hyperplasias [1].
• The high frequency of loss of heterozygosity (LOH) in epithelial cells of mammary ductal carcinoma in situ (DCIS) and IDC is a well known phenomenon, whereas the genetic abnormalities in the mammary stroma and its influence on the epithelial component have not been sufficiently studied [2].
• ER+ human breast cancer cell lines MCF-7 and T-47D, using MDA-MB-231 as ER-; control, and murine mammary ductal carcinomas MC4-L2, MC4-L3, and MC7-L1, were compared for their in vivo growth rate and retention of ER+ status [3].
• Two estrogen sulfatases, arylsulfatase C-estrone sulfatase (ASC-ES) and d-equilenin sulfatase (EqS) were demonstrated histochemically in the normal human female breast, in benign breast diseases and in infiltrating mammary ductal carcinomas to study their significance in the pathogenesis of epithelial proliferations [4].

High impact information on Carcinoma, Ductal, Breast

• p53 in Mammary ductal carcinoma in situ, mutations in high-grade lesions only [5]?
• Somatic mutations and altered expression of the candidate tumor suppressors CSNK1 epsilon, DLG1, and EDD/hHYD in mammary ductal carcinoma [6].
• Hyperimmune sera increased complement-mediated cytotoxicity versus P3X63 myeloma cells and a marked IgG differential reactivity against human mammary ductal carcinoma samples [7].
• p21, p27 and p53 in estrogen and antiprogestin-induced tumor regression of experimental mouse mammary ductal carcinomas [8].
• p53 protein expression in mammary ductal carcinoma in situ: relationship to immunohistochemical expression of estrogen receptor and c-erbB-2 protein [9].

Chemical compound and disease context of Carcinoma, Ductal, Breast

• Captopril modulates hormone receptor concentration and inhibits proliferation of human mammary ductal carcinoma cells in culture [10].
• Using medroxyprogesterone acetate (MPA) as a carcinogen, we were able to induce in BALB/c female mice, several progestin-dependent mammary ductal carcinomas that regress completely with estrogen or antiprogestins and are maintained by serial transplantations in syngeneic mice [11].

Gene context of Carcinoma, Ductal, Breast

• Mammary ductal carcinoma developed earlier in Wnt-1 TG, Pten+/- mice than in mice bearing either genetic change alone, and showed frequent loss of the remaining wild-type PTEN allele [12].
• Expression of maspin is up-regulated during the progression of mammary ductal carcinoma [13].
• Prognostic value of immunocytochemical estimation of estrogen receptor (ER) and of pS2 estrogen-dependent protein in cells of mammary ductal carcinoma. Analysis of five-year course of the disease [14].
• Analysis of estrogen receptor (ER) and estrogen-dependent pS2 protein expression in cells of mammary ductal carcinoma [15].
• In a series of 46 cases of primary mammary ductal carcinoma, immunohistochemical markers of differentiation (casein, human placental lactogen, alphalactalbumin, pregnancy specific beta-1 glycoprotein, secretory component, CEA, and peanut lectin agglutinins [PLA]), were quantitated via point-counting [16].

References