Glucocorticoid receptors in mouse mammary tumors. Specific binding to nuclear components

Biochemistry ◽  
1975 ◽  
Vol 14 (2) ◽  
pp. 437-444 ◽  
Author(s):  
G. Shyamala
Keyword(s):  
Glucocorticoid Receptors ◽  
Specific Binding ◽  
Mammary Tumors ◽  
Mouse Mammary Tumors

Great Increase of Numbers of Virus Particles by Irradiating C3H Mouse Mammary Tumors Transplanted into Male Mice

1972 ◽  
Vol 30 ◽  
pp. 272-273
Author(s):  
P. J. Melnick ◽  
J. W. Cha ◽  
E. Samouhos
Keyword(s):  
Subcutaneous Tissue ◽  
Mammary Tumors ◽  
The Body ◽  
X Ray ◽  
Virus Particles ◽  
Mouse Mammary Tumors ◽  
Transplantable Tumors ◽  
C3h Mice ◽  
Cobalt Radiation ◽  
Enzyme Changes

Spontaneous mammary tumors in females of a high tumor strain of C3H mice were cut into small fragments that were Implanted into the subcutaneous tissue of the back of males of the same strain, where they grew as transplantable tumors. When about Cm. In diameter daily fractional radiation was begun, applied to the tumors, the rest of the body being shielded by a lead shield. Two groups were treated with 150 and 200 r X-ray dally, of half value layer 0.6mm. copper; a third group was treated with 500 r cobalt radiation dally. The primary purpose was to examine the enzyme changes during radiation, with histochemlcal technics.

scholarly journals Fgf10 is an oncogene activated by MMTV insertional mutagenesis in mouse mammary tumors and overexpressed in a subset of human breast carcinomas

Oncogene ◽  
2004 ◽  
Vol 23 (36) ◽  
pp. 6047-6055 ◽  
Author(s):  
Vassiliki Theodorou ◽  
Mandy Boer ◽  
Britta Weigelt ◽  
Jos Jonkers ◽  
Martin van der Valk ◽  
...  
Keyword(s):  
Insertional Mutagenesis ◽  
Mammary Tumors ◽  
Breast Carcinomas ◽  
Human Breast ◽  
Human Breast Carcinomas ◽  
Mouse Mammary Tumors

scholarly journals Telomerase activation in mouse mammary tumors: lack of detectable telomere shortening and evidence for regulation of telomerase RNA with cell proliferation.

1996 ◽  
Vol 16 (7) ◽  
pp. 3765-3772 ◽  
Author(s):  
D Broccoli ◽  
L A Godley ◽  
L A Donehower ◽  
H E Varmus ◽  
T de Lange
Keyword(s):  
Cell Proliferation ◽  
Tumor Development ◽  
Mammary Tumorigenesis ◽  
Mammary Tumors ◽  
Mammary Glands ◽  
Telomerase Activity ◽  
Telomerase Rna ◽  
Proliferating Cells ◽  
Telomere Shortening ◽  
Mouse Mammary Tumors

Activation of telomerase in human cancers is thought to be necessary to overcome the progressive loss of telomeric DNA that accompanies proliferation of normal somatic cells. According to this model, telomerase provides a growth advantage to cells in which extensive terminal sequence loss threatens viability. To test these ideas, we have examined telomere dynamics and telomerase activation during mammary tumorigenesis in mice carrying a mouse mammary tumor virus long terminal repeat-driven Wnt-1 transgene. We also analyzed Wnt-1-induced mammary tumors in mice lacking p53 function. Normal mammary glands, hyperplastic mammary glands, and mammary carcinomas all had the long telomeres (20 to 50 kb) typical of Mus musculus and did not show telomere shortening during tumor development. Nevertheless, telomerase activity and the RNA component of the enzyme were consistently upregulated in Wnt-1-induced mammary tumors compared with normal and hyperplastic tissues. The upregulation of telomerase activity and RNA also occurred during tumorigenesis in p53-deficient mice. The expression of telomerase RNA correlated strongly with histone H4 mRNA in all normal tissues and tumors, indicating that the RNA component of telomerase is regulated with cell proliferation. Telomerase activity in the tumors was elevated to a greater extent than telomerase RNA, implying that the enzymatic activity of telomerase is regulated at additional levels. Our data suggest that the mechanism of telomerase activation in mouse mammary tumors is not linked to global loss of telomere function but involves multiple regulatory events including upregulation of telomerase RNA in proliferating cells.

Specific activation of the cellular Harvey-ras oncogene in dimethylbenzanthracene-induced mouse mammary tumors

1986 ◽  
Vol 6 (11) ◽  
pp. 4104-4108
Author(s):  
S Dandekar ◽  
S Sukumar ◽  
H Zarbl ◽  
L J Young ◽  
R D Cardiff
Keyword(s):  
Mammary Tumors ◽  
3T3 Cells ◽  
Mouse Mammary Tumor ◽  
Mouse Mammary Tumors ◽  
Transforming Activity ◽  
Radiation Induced ◽  
Genomic Dnas ◽  
Nih 3T3 ◽  
Adenosine Nucleotide ◽  
Nih 3T3 Cells

Genomic DNAs from dimethylbenzanthracene-induced BALB/c mouse mammary tumors arising from the transplantable hyperplastic outgrowth (HPO) line designated DI/UCD transformed NIH 3T3 cells upon transfection. Transforming activity was attributed to the presence of activated Harvey ras-1 oncogenes containing an A----T transversion at the middle adenosine nucleotide in codon 61. DNAs from untreated DI/UCD HPO cells and radiation-induced and spontaneous mammary tumors from the DI/UCD HPO line failed to transform NIH 3T3 cells. The results indicated that the mutation activation of Harvey ras-1 oncogenes was specific to dimethylbenzanthracene treatment in the mouse mammary tumor system.

scholarly journals Dexamethasone modulates the metabolism of type IV collagen and fibronectin in human basement-membrane-forming fibrosarcoma (HT-1080) cells

1987 ◽  
Vol 245 (1) ◽  
pp. 235-241 ◽  
Author(s):  
A Oikarinen ◽  
T Salo ◽  
L Ala-Kokko ◽  
K Tryggvason
Keyword(s):  
Total Protein ◽  
Messenger Rna ◽  
Collagen Synthesis ◽  
Glucocorticoid Receptors ◽  
Type Iv Collagen ◽  
Cell Layer ◽  
Specific Binding ◽  
Specific Radioactivity ◽  
Filtration Method ◽  
Type Iv

The effect of dexamethasone on the synthesis and degradation of type IV collagen was studied in human fibrosarcoma cells, HT-1080. A dexamethasone concentration as low as 0.1 microM markedly increased collagen synthesis in HT-1080 cells labelled with [14C]proline. The increase in type IV collagen synthesis was not specific, since total protein synthesis was also increased. Further studies indicated that part of the increase was due to an increase in the specific radioactivity of the intracellular proline pool, after dexamethasone treatment. In fact, with dexamethasone concentrations of 0.1-10 microM the relative collagen synthesis was decreased, indicating that synthesis of other protein was increased more than that of type IV collagen. This was also confirmed by measuring the relative amount of type IV collagen RNA by using recombinant plasmid cDNA specific for the human procollagen pro alpha l (IV) RNA. The results indicated that relative collagen synthesis and the relative amount of type IV collagen messenger RNA was decreased similarly, indicating that dexamethasone affected type IV collagen synthesis at the pre-translational level. The dexamethasone-induced effect on total protein and collagen synthesis was maximal after 12-24 h. Dexamethasone induced a marked accumulation of collagen into the cell layer, leading to diminished deposition of soluble collagen into the medium. Since bacterial-collagenase treatment of the cell layer drastically decreased the collagen content of the dexamethasone-treated cells, this indicates that dexamethasone caused an accumulation of collagen into the extracellular matrix of the cell layer. In contrast, the amount of fibronectin was markedly increased in the medium. Dexamethasone decreased the type IV collagen-degrading activity in HT-1080 cells. The HT-1080 cells contained glucocorticoid receptors, as demonstrated by two different methods: by a whole-cell binding assay and by using a cytosol-gel-filtration method. The number of specific binding sites was similar to that in human skin fibroblasts. In conclusion, glucocorticoids affect the metabolism of type IV collagen and fibronectin in HT-1080 cells, and, since these cells contain specific glucocorticoid receptors, the effects are apparently receptor-mediated.

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