High frequency variation in mammary tumor virus expression in cell culture

Cell ◽  
1976 ◽  
Vol 8 (1) ◽  
pp. 87-93 ◽  
Author(s):  
Wade P. Parks ◽  
Elizabeth S. Hubbell ◽  
Robert J. Goldberg ◽  
Frank J. O'Neill ◽  
Edward M. Scolnick
Virology ◽  
1977 ◽  
Vol 82 (1) ◽  
pp. 232-236 ◽  
Author(s):  
James A. Strauchen ◽  
Nathaniel A. Young ◽  
Robert M. Friedman

2001 ◽  
Vol 75 (23) ◽  
pp. 11886-11890 ◽  
Author(s):  
Jennifer Czarneski ◽  
Jennifer Meyers ◽  
Tao Peng ◽  
Valsamma Abraham ◽  
Rosemarie Mick ◽  
...  

ABSTRACT The mouse mammary tumor virus (MMTV) superantigen induces T-cell production of cytokines, such as interleukin-4, which in turn increase MMTV transcription. However, interleukin-4 is not required for in vivo virus spread, because mice lacking interleukin-4 or the STAT6 transcription factor showed wild-type infection of lymphoid and mammary tissue. In spite of this, mammary tumor incidence was decreased in STAT6 null mice.


1977 ◽  
Vol 146 (5) ◽  
pp. 1206-1220 ◽  
Author(s):  
W E Heston ◽  
W P Parks

Mammary tumorigenesis in genetic crosses between the high mammary tumor incidence GR and the low incidence C57BL mouse strains is highly correlated with murine mammary tumor virus expression in milk. Although the F1 and first backcross females had a mammary tumor incidence which was consistent with a single dominant gene segregation, the tumor incidence in the critical second backcross segregants disproved the single gene hypothesis. Genetic factors were clearly involved in regulation of virus expression which in turn correlated with both tumor incidence and tumor latency; these complex phenotypes are however best explained as threshold or quasicontinuous characters. As predicted from this model, the age specific incidence of mammary tumors showed a broad peak at 14-19 mo of age with no evidence of an early or late phase. Hematopoietic tumors showed no correlation with virus expression or mammary tumorigenesis suggesting different etiologies for these tumors.


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