Subject(s)
Humans , Female , Animals , Mice , Biological Treatment , Breast Neoplasms/drug therapy , Breast Neoplasms/immunology , Breast Neoplasms/therapy , In Vitro Techniques , Neoplasm Metastasis , Estrogens/therapeutic use , Exotoxins/therapeutic use , Epidermal Growth Factor , Genes, erbB-2 , RNA, Complementary/isolation & purification , Tamoxifen/therapeutic useSubject(s)
Humans , Animals , Female , Breast Neoplasms/drug therapy , Breast Neoplasms/therapy , Capillaries , Growth Substances/adverse effects , Angiogenesis Inhibitors , Molecular Biology , Neoplasm Metastasis , Prognosis , Antigens, Differentiation/classification , Apoptosis/drug effects , Biological Treatment , Cytotoxicity, Immunologic , Drug Resistance, Neoplasm , Endothelial Growth Factors , Heparin/pharmacokinetics , Immunohistochemistry , Necrosis/physiopathology , Neoplasm Recurrence, Local , Poisons/therapeutic use , Pentosan Sulfuric Polyester/pharmacokinetics , Prostatic Neoplasms/therapy , Heat-Shock Proteins/therapeutic useSubject(s)
Humans , Female , Animals , Mice , In Vitro Techniques , Breast Neoplasms/therapy , Breast Neoplasms/drug therapy , Breast Neoplasms/immunology , Neoplasm Metastasis , Biological Treatment , Estrogens/therapeutic use , Tamoxifen/therapeutic use , Epidermal Growth Factor , Genes, erbB-2 , Exotoxins/therapeutic use , RNA, Complementary/isolation & purificationSubject(s)
Humans , Animals , Female , Capillaries , Angiogenesis Inhibitors , Neoplasm Metastasis , Prognosis , Molecular Biology , Growth Substances/adverse effects , Breast Neoplasms/therapy , Breast Neoplasms/drug therapy , Heparin/pharmacokinetics , Pentosan Sulfuric Polyester/pharmacokinetics , Prostatic Neoplasms/therapy , Endothelial Growth Factors , Neoplasm Recurrence, Local , Poisons/therapeutic use , Biological Treatment , Apoptosis/drug effects , Necrosis/physiopathology , Heat-Shock Proteins/therapeutic use , Drug Resistance, Neoplasm , Antigens, Differentiation/classification , Immunohistochemistry , Cytotoxicity, ImmunologicABSTRACT
We investigated the expression of transforming growth factors beta 1 and alpha (TGF-beta 1, TGF-alpha) in hormone-responsive (MPA-R) and unresponsive (MPA-U) tumor lines obtained from medroxyprogesterone acetate (MPA)-induced mammary adenocarcinomas in BALB/c mice. The tumors were transplanted into MPA-treated and untreated mice. TGF-beta 1 gene expression was observed in the MPA-R lines growing in untreated animals, but not in MPA-treated mice. TGF-beta 1 mRNA was not detected in the MPA-U tumor lines growing in either MPA-treated or untreated animals. In MPA-R lines the levels of TGF-beta 1 expression were inversely correlated to growth rate. High-affinity TGF-beta 1 receptors were present in the MPA-R tumors. These results suggest that one of the mechanisms by which MPA exerts its proliferative effect on MPA-R tumor lines is inhibition of the expression of TGF-beta 1. Thus, the lack of expression of TGF-beta 1 in MPA-U tumors may be related to the acquisition of autonomous growth.