Selective amplification of mouse mammary tumor virus in mammary tumors of GR mice.

1980 ◽  
Vol 36 (1) ◽  
pp. 109-114 ◽  
Author(s):  
T G Fanning ◽  
J P Puma ◽  
R D Cardiff
Author(s):  
T. Kodama ◽  
W. C. Williams ◽  
R. L. Hales ◽  
L. Dmochowski

Morphological, biological, and immunological studies indicate a possible interrelationship between mouse mammary tumor virus and leukemia virus in the development of mouse mammary tumors. Electron microscope studies have shown the presence of both mouse mammary tumor virus (type B) particles and mouse leukemia virus (type C) particles in mouse milk, in tissues, and in tissue cultures from spontaneous and induced mouse mammary tumors (Dmochowski, L., et; al.: Carcinogenesis, A Broad Critique, Williams and Wilkins Co., Baltimore, p.211, 1967;., Dmochowski, L., et al.: J.Nat. Cancer Inst., 40:1339, 1968).


1980 ◽  
Vol 152 (3) ◽  
pp. 712-719 ◽  
Author(s):  
R Nusse ◽  
J de Moes ◽  
J Hilkens ◽  
R van Nie

The GR/Mtv-2- mouse strain is congenic to the GR strain but lacks the Mtv-2 gene for high amounts of mouse mammary tumor virus (MMTV) virion particles in the milk and early mammary tumors. With a sensitive competition radioimmunoassay for individual viral proteins of MMTV, substantial amounts of the gag proteins p27 and p10 could still be detected in extracts of the mammary glands of GR/Mtv-2- mice, but essentially no viral envelope antigens. The genetic transmission of the MMTV gag expression in the GR/Mtv-2- strain was investigated. In a cross with the virus-negative BALB/c strain, the MMTV p27 expression behaved as a dominant feature. Double backcross analysis proved that the p27 expression was governed by a single gene located on chromosome 11, cloe to the Es-3 locus. The gene was thereby not allelic to any of the previously described MMTV induction genes, Mtv-1 and Mtv-2, and is therefore called Mtv-3. It is concluded that the total MMTV expression in the GR strain is under control of two separate loci, Mtv-2 on chromosome 18, inducing high levels of complete virus particles and also early mammary tumors; and Mtv-3 on chromosome 11, coding for partial MMTV expression.


Virology ◽  
1981 ◽  
Vol 113 (1) ◽  
pp. 119-129 ◽  
Author(s):  
Janet I. Macinnes ◽  
Edwin C.M. Lee Chan ◽  
Dean H. Percy ◽  
Vincent L. Morris

1996 ◽  
Vol 16 (10) ◽  
pp. 5726-5736 ◽  
Author(s):  
W J Muller ◽  
C L Arteaga ◽  
S K Muthuswamy ◽  
P M Siegel ◽  
M A Webster ◽  
...  

Transgenic mice expressing either the neu proto-oncogene or transforming growth factor (TGF-alpha) in the mammary epithelium develop spontaneous focal mammary tumors that occur after a long latency. Since the epidermal growth factor receptor (EGFR) and Neu are capable of forming heterodimers that are responsive to EGFR ligands such as TGF-alpha, we examined whether coexpression of TGF-alpha and Neu in mammary epithelium could cooperate to accelerate the onset of mammary tumors. To test this hypothesis, we interbred separate transgenic strains harboring either a mouse mammary tumor virus/TGF-alpha or a mouse mammary tumor virus/neu transgene to generate bitransgenic mice that coexpress TGF-alpha and neu in the mammary epithelium. Female mice coexpressing TGF-alpha and neu developed multifocal mammary tumors which arose after a significantly shorter latency period than either parental strain alone. The development of these mammary tumors was correlated with the tyrosine phosphorylation of Neu and the recruitment of c-Src to the Neu complex. Immunoprecipitation and immunoblot analyses with EGFR- and Neu-specific antisera, however, failed to detect physical complexes of these two receptors. Taken together, these observations suggest that Neu and TGF-alpha cooperate in mammary tumorigenesis through a mechanism involving Neu and EGFR transactivation.


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