On the Mechanism of Carcinogenesis by Mouse Mammary Tumor Virus

1987 ◽  
pp. 307-319 ◽  
Author(s):  
Gordon Peters ◽  
Clive Dickson
Keyword(s):  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus ◽  
Mechanism Of Carcinogenesis

Electron Microscopy of the Nucleic Acid of Mouse Mammary Tumor Virus

1968 ◽  
Vol 26 ◽  
pp. 22-23
Author(s):  
N. H. Sarkar ◽  
Dan H. Moore
Keyword(s):  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Ammonium Acetate ◽  
Dry Weight ◽  
Mouse Tumor ◽  
Mammary Tumor Virus ◽  
Rna Molecules ◽  
Mouse Mammary Tumor ◽  
Tumor Virus ◽  
The Subject

Mouse mammary tumor virus (MTV) is believed to contain about 0.8% single stranded ribonucleic acid (RNA). This value of RNA content was estimated on a dry weight basis. The subject of this report is an attempt to visualize the RNA molecules of MTV particles.MTV particles were isolated from RIII mouse (tumor incidence approximately 80%) milk according to the method described by Lyons and Moore. Purified virions from 5 ml of milk were finally suspended in 0.2 ml of PBS, pH 7.4 and was mixed with an equal volume of pronase (5 mg/ml). This mixture was incubated at 37°C for an hour. RNA was extracted three times using freshly prepared cold phenol. It was then treated three times with cold ethyl ether to remove any trace of phenol. The RNA thus extracted was divided into two parts. One part was diluted four fold with 8M urea to avoid aggregation of the molecules. The other part was left untreated. Both samples were then mixed with an equal volume of 1M ammonium acetate, adjusted to pH 8.0 with NH3 containing chymotrypsin at a concentration of 0.01%.

A novel V beta 2-specific endogenous mouse mammary tumor virus which is capable of producing a milk-borne exogenous virus.

1995 ◽  
Vol 69 (11) ◽  
pp. 7269-7273 ◽  
Author(s):  
N Niimi ◽  
W Wajjwalku ◽  
Y Ando ◽  
N Nakamura ◽  
M Ueda ◽  
...  
Keyword(s):  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Mammary Tumor Virus ◽  
Exogenous Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus ◽  
Beta 2

Mouse mammary tumor virus (MMTV) antigen(s) are present on B lymphocytes of BALB/c mice

1979 ◽  
Vol 24 (6) ◽  
pp. 813-818 ◽  
Author(s):  
Vijaya Charyulu ◽  
M. Michael Sigel ◽  
Donald L. Durden ◽  
Diana M. Lopez
Keyword(s):  
B Lymphocytes ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus

scholarly journals Heregulin Co-opts PR Transcriptional Action Via Stat3 Role As a Coregulator to Drive Cancer Growth

2015 ◽  
Vol 29 (10) ◽  
pp. 1468-1485 ◽  
Author(s):  
Cecilia J. Proietti ◽  
Franco Izzo ◽  
María Celeste Díaz Flaqué ◽  
Rosalía Cordo Russo ◽  
Leandro Venturutti ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Signaling Pathways ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Cancer Growth ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus ◽  
Virus Promoter

Abstract Accumulated findings have demonstrated the presence of bidirectional interactions between progesterone receptor (PR) and the ErbB family of receptor tyrosine kinases signaling pathways in breast cancer. We previously revealed signal transducer and activator of transcription 3 (Stat3) as a nodal convergence point between said signaling pathways proving that Stat3 is activated by one of the ErbBs' ligands, heregulin (HRG)β1 via ErbB2 and through the co-option of PR as a signaling molecule. Here, we found that HRGβ1 induced Stat3 recruitment to the promoters of the progestin-regulated cell cycle modulators Bcl-XL and p21CIP1 and also stimulated Stat3 binding to the mouse mammary tumor virus promoter, which carries consensus progesterone response elements. Interestingly, HRGβ1-activated Stat3 displayed differential functions on PR activity depending on the promoter bound. Indeed, Stat3 was required for PR binding in bcl-X, p21CIP1, and c-myc promoters while exerting a PR coactivator function on the mouse mammary tumor virus promoter. Stat3 also proved to be necessary for HRGβ1-induced in vivo tumor growth. Our results endow Stat3 a novel function as a coregulator of HRGβ1-activated PR to promote breast cancer growth. These findings underscore the importance of understanding the complex interactions between PR and other regulatory factors, such as Stat3, that contribute to determine the context-dependent transcriptional actions of PR.

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