Mouse mammary tumor virus and murine leukemia virus cell surface antigens on virus producer and nonproducer mammary epithelial tumor cells

Virology ◽  
1978 ◽  
Vol 88 (2) ◽  
pp. 379-383 ◽  
Author(s):  
Gerald Schochetman ◽  
Donald L. Fine ◽  
Richard J. Massey
1998 ◽  
Vol 72 (2) ◽  
pp. 1699-1703 ◽  
Author(s):  
Robert M. Saller ◽  
Feride Öztürk ◽  
Brian Salmons ◽  
Walter H. Günzburg

ABSTRACT Mouse mammary tumor virus (MMTV)-based vectors are characterized by low titers. In an effort to transfer MMTV-specific regulation of gene expression to a more efficient murine leukemia virus (MLV) vector, we have replaced the complete 3′ U3 region of MLV with the complete U3 region of MMTV. Virus titers were not significantly affected by this modification, there was no impairment of reverse transcription and integration, and after infection of cells, the MMTV promoter is duplicated and translocated to the 5′ long terminal repeat, resulting in glucocorticoid-regulatable RNA expression.


Development ◽  
1998 ◽  
Vol 125 (10) ◽  
pp. 1921-1930 ◽  
Author(s):  
E.C. Kordon ◽  
G.H. Smith

Any epithelial portion of a normal mouse mammary gland can reproduce an entire functional gland when transplanted into an epithelium-free mammary fat pad. Mouse mammary hyperplasias and tumors are clonal dominant populations and probably represent the progeny of a single transformed cell. Our study provides evidence that single multipotent stem cells positioned throughout the mature fully developed mammary gland have the capacity to produce sufficient differentiated progeny to recapitulate an entire functional gland. Our evidence also demonstrates that these stem cells are self-renewing and are found with undiminished capacities in the newly regenerated gland. We have taken advantage of an experimental model where mouse mammary tumor virus infects mammary epithelial cells and inserts a deoxyribonucleic acid copy(ies) of its genome during replication. The insertions occur randomly within the somatic genome. CzechII mice have no endogenous nucleic acid sequence homology with mouse mammary tumor virus; therefore all viral insertions may be detected by Southern analysis provided a sufficient number of cells contain a specific insertional event. Transplantation of random fragments of infected CzechII mammary gland produced clonal-dominant epithelial populations in epithelium-free mammary fat pads. Serial transplantation of pieces of the clonally derived outgrowths produced second generation glands possessing the same viral insertion sites providing evidence for self-renewal of the original stem cell. Limiting dilution studies with cell cultures derived from third generation clonal outgrowths demonstrated that three multipotent but distinct mammary epithelial progenitors were present in clonally derived mammary epithelial populations. Estimation of the potential number of multipotent epithelial cells that may be evolved from an individual mammary-specific stem cell by self-renewal is in the order of 10(12)-10(13). Therefore, one stem cell might easily account for the renewal of mammary epithelium over several transplant generations.


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).


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