|1.||Sato, K: 1 article (01/2000)|
|2.||Wierzba, K: 1 article (01/2000)|
|3.||Toko, T: 1 article (01/2000)|
|4.||Yamada, Y: 1 article (01/2000)|
|5.||Saito, H: 1 article (01/2000)|
|6.||Shibata, J: 1 article (01/2000)|
|7.||Lykkesfeldt, A E: 1 article (01/2000)|
|8.||Hashimoto, A: 1 article (01/2000)|
|9.||Fujioka, A: 1 article (01/2000)|
|1.||Leydig Cell Tumor
01/01/1994 - "Much higher levels of DP-TAT-59 and DM-DP-TAT-59 were shown in tumors (target tissues of estrogen) as compared with muscles (nontarget tissues of estrogen) or serum. "
01/01/1995 - "After oral administration of the drugs, DP-TAT-59, one of the main metabolites of TAT-59, was found in 10- to 15-fold higher concentrations in both the tumor and blood compared to 4-OH-TAM, an active metabolite of TAM. "
01/01/2000 - "DP-TAT-59 significantly inhibited the proliferation of estrogen receptor-positive MCF-7 and T-47D tumor cells in the presence of 1 nM estradiol. "
05/01/1998 - "DP-TAT-59 and DM-DP-TAT-59, major metabolites of TAT-59 detected in blood after oral administration in the patients, exhibited equal growth-inhibitory activity against human mammary tumor xenograft, meaning the antitumor activity of TAT-59 may equally depend on these two metabolites. "
01/01/1994 - "A serum concentration of DP-TAT-59 or DM-DP-TAT-59 corresponding to the physiologic levels of serum estradiol in premenopausal women was sufficient to inhibit the estrogen-stimulated growth of MCF-7 tumors in mice. "
|3.||Breast Neoplasms (Breast Cancer)
05/01/1998 - "DP-TAT-59, an active metabolite of miproxifene phosphate (TAT-59), showed a strong anti-proliferating activity against ER-positive human mammary carcinoma cell lines, MCF-7 and T-47D, in the presence of 1 nM of estradiol. "
01/01/1997 - "Antiestrogenic activity of DP-TAT-59, an active metabolite of TAT-59 against human breast cancer."
01/01/1997 - "These findings suggest that at least a part of the growth suppressive ability of DP-TAT-59 against human mammary carcinoma might depend on the production of growth inhibitory factors and/or the suppression of production of growth factors from ER-positive cells, and that the production of growth inhibitory factors might be stimulated by ER complexes with antiestrogens rather than with estrogen."
|4.||Intercellular Signaling Peptides and Proteins (Growth Factors)
|5.||Estrogen Receptor Modulators (Antiestrogen)
|2.||Heterologous Transplantation (Xenotransplantation)