The Experts below are selected from a list of 153 Experts worldwide ranked by ideXlab platform
Susan R. Ross - One of the best experts on this subject based on the ideXlab platform.
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Interleukin-4 Up-Regulates Mouse Mammary Tumor Virus Expression yet Is Not Required for In Vivo Virus Spread
Journal of virology, 2001Co-Authors: Jennifer Czarneski, Jennifer L. Meyers, Tao Peng, Valsamma Abraham, Rosemarie Mick, Susan R. RossAbstract: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.
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Expression of mouse Mammary Tumor virus envelope protein does not prevent superinfection in vivo or in vitro.
Virology, 1999Co-Authors: John L. Dzuris, Wei Zhu, Denis Kapkov, Tatyana V. Golovkina, Susan R. RossAbstract:Inbred mice expressing endogenous mouse Mammary Tumor virus envelope proteins can be infected with exogenous virus, and the Mammary Tumors that develop in these mice usually have many proviruses integrated in their genomes, indicating that this virus is not subject to receptor interference. We show here that transgenic mice expressing an exogenous mouse Mammary Tumor virus (C3H) envelope protein can still be infected with this virus. Moreover, cultured Mammary gland cells expressing the mouse Mammary Tumor virus (C3H) envelope protein can be superinfected with pseudotyped viruses bearing that same protein. Thus cellular expression of the mouse Mammary Tumor virus envelope protein does not block superinfection in vivo or in vitro.
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coexpression of exogenous and endogenous mouse Mammary Tumor virus rna in vivo results in viral recombination and broadens the virus host range
Journal of Virology, 1994Co-Authors: Tatyana V. Golovkina, Aron B Jaffe, Susan R. RossAbstract:Abstract Mouse Mammary Tumor virus is a replication-competent B-type murine retrovirus responsible for Mammary gland Tumorigenesis in some strains of laboratory mice. Mouse Mammary Tumor virus is transmitted horizontally through the milk (exogenous or milk-borne virus) to susceptible offspring or vertically through the germ line (endogenous provirus). Exogenously acquired and some endogenous mouse Mammary Tumor viruses are expressed at high levels in lactating Mammary glands. We show here that there is packaging of the endogenous Mtv-1 virus, which is expressed at high levels in the lactating Mammary glands of C3H/HeN mice, by the virions of exogenous C3H mouse Mammary Tumor virus [MMTV(C3H)]. The Mammary Tumors induced in C3H/HeN mice infected with exogenous MMTV (C3H) virus contained integrated copies of recombinant virus containing a region of the env gene from an endogenous virus. This finding indicates that there was copackaging of the Mtv-1 and MMTV(C3H) RNAs in the same virions. Moreover, because Mtv-1 encodes a superantigen protein with a V beta specificity different from that encoded by the exogenous virus, the packaging of Mtv-1 results in an infectious virus with a broader host range than MMTV(C3H).
Tatyana V. Golovkina - One of the best experts on this subject based on the ideXlab platform.
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Expression of mouse Mammary Tumor virus envelope protein does not prevent superinfection in vivo or in vitro.
Virology, 1999Co-Authors: John L. Dzuris, Wei Zhu, Denis Kapkov, Tatyana V. Golovkina, Susan R. RossAbstract:Inbred mice expressing endogenous mouse Mammary Tumor virus envelope proteins can be infected with exogenous virus, and the Mammary Tumors that develop in these mice usually have many proviruses integrated in their genomes, indicating that this virus is not subject to receptor interference. We show here that transgenic mice expressing an exogenous mouse Mammary Tumor virus (C3H) envelope protein can still be infected with this virus. Moreover, cultured Mammary gland cells expressing the mouse Mammary Tumor virus (C3H) envelope protein can be superinfected with pseudotyped viruses bearing that same protein. Thus cellular expression of the mouse Mammary Tumor virus envelope protein does not block superinfection in vivo or in vitro.
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coexpression of exogenous and endogenous mouse Mammary Tumor virus rna in vivo results in viral recombination and broadens the virus host range
Journal of Virology, 1994Co-Authors: Tatyana V. Golovkina, Aron B Jaffe, Susan R. RossAbstract:Abstract Mouse Mammary Tumor virus is a replication-competent B-type murine retrovirus responsible for Mammary gland Tumorigenesis in some strains of laboratory mice. Mouse Mammary Tumor virus is transmitted horizontally through the milk (exogenous or milk-borne virus) to susceptible offspring or vertically through the germ line (endogenous provirus). Exogenously acquired and some endogenous mouse Mammary Tumor viruses are expressed at high levels in lactating Mammary glands. We show here that there is packaging of the endogenous Mtv-1 virus, which is expressed at high levels in the lactating Mammary glands of C3H/HeN mice, by the virions of exogenous C3H mouse Mammary Tumor virus [MMTV(C3H)]. The Mammary Tumors induced in C3H/HeN mice infected with exogenous MMTV (C3H) virus contained integrated copies of recombinant virus containing a region of the env gene from an endogenous virus. This finding indicates that there was copackaging of the Mtv-1 and MMTV(C3H) RNAs in the same virions. Moreover, because Mtv-1 encodes a superantigen protein with a V beta specificity different from that encoded by the exogenous virus, the packaging of Mtv-1 results in an infectious virus with a broader host range than MMTV(C3H).
William J Muller - One of the best experts on this subject based on the ideXlab platform.
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akt1 and akt2 play distinct roles in the initiation and metastatic phases of Mammary Tumor progression
Cancer Research, 2009Co-Authors: Rachelle L Dillon, Bryan T. Hennessy, Gordon B. Mills, Richard Marcotte, James R Woodgett, William J MullerAbstract:The phosphatidylinositol 3-kinase (PI3K)/Akt survival pathway is often dysregulated in cancer. Our previous studies have shown that coexpression of activated Akt1 with activated ErbB2 or polyoma virus middle T antigen uncoupled from the PI3K pathway (PyVmT Y315/322F) accelerates Mammary Tumor development but cannot rescue the metastatic phenotype associated with these models. Here, we report the generation of transgenic mice expressing activated Akt2 in the Mammary epithelium. Like the mouse Mammary Tumor virus-Akt1 strain, Mammary-specific expression of Akt2 delayed Mammary gland involution. However, in contrast to Akt1, coexpression of Akt2 with activated ErbB2 or PyVmT Y315/322F in the Mammary glands of transgenic mice did not affect the latency of Tumor development. Strikingly, Akt2 coexpresssion markedly increased the incidence of pulmonary metastases in both Tumor models, demonstrating a unique role in Tumor progression. Together, these observations argue that these highly conserved kinases have distinct biological and biochemical outputs that play opposing roles in Mammary Tumor induction and metastasis. [Cancer Res 2009;69(12):5057–64]
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Mammary epithelial specific disruption of the focal adhesion kinase blocks Mammary Tumor progression
Proceedings of the National Academy of Sciences of the United States of America, 2007Co-Authors: Hicham Lahlou, Robert D. Cardiff, Virginie Sanguingendreau, Dongmei Zuo, Gordon W Mclean, Margaret C Frame, William J MullerAbstract:Elevated expression and activation of the focal adhesion kinase (FAK) occurs in a large proportion of human breast cancers. Although several studies have implicated FAK as an important signaling molecule in cell culture systems, evidence supporting a role for FAK in Mammary Tumor progression is lacking. To directly assess the role of FAK in this process, we have used the Cre/loxP recombination system to disrupt FAK function in the Mammary epithelium of a transgenic model of breast cancer. Using this approach, we demonstrate that FAK expression is required for the transition of premalignant hyperplasias to carcinomas and their subsequent metastases. This dramatic block in Tumor progression was further correlated with impaired Mammary epithelial proliferation. These observations provide direct evidence that FAK plays a critical role in Mammary Tumor progression.
Sylvie Ménard - One of the best experts on this subject based on the ideXlab platform.
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Prevention of spontaneous neu-expressing Mammary Tumor development in mice transgenic for rat proto-neu by DNA vaccination
Gene Therapy, 2001Co-Authors: Serenella M. Pupa, Annamaria Invernizzi, Stefania Forti, E. Di Carlo, Piero Musiani, Patrizia Nanni, Pier Luigi Lollini, Raffaella Meazza, Silvano Ferrini, Sylvie MénardAbstract:Prevention of spontaneous neu-expressing Mammary Tumor development in mice transgenic for rat proto-neu by DNA vaccination
Hans Achaorbea - One of the best experts on this subject based on the ideXlab platform.
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preferential infection of immature dendritic cells and b cells by mouse Mammary Tumor virus
Journal of Immunology, 2002Co-Authors: Sonia Vacheron, Sanjiv A Luther, Hans AchaorbeaAbstract:Until now it was thought that the retrovirus mouse Mammary Tumor virus preferentially infects B cells, which thereafter proliferate and differentiate due to superantigen-mediated T cell help. We describe in this study that dendritic cells are infectable at levels comparable to B cells in the first days after virus injection. Moreover, IgM knockout mice have chronically deleted superantigen-reactive T cells after MMTV injection, indicating that superantigen presentation by dendritic cells is sufficient for T cell deletion. In both subsets initially only few cells were infected, but there was an exponential increase in numbers of infected B cells due to superantigen-mediated T cell help, explaining that at the peak of the response infection is almost exclusively found in B cells. The level of infection in vivo was below 1 in 1000 dendritic cells or B cells. Infection levels in freshly isolated dendritic cells from spleen, Langerhans cells from skin, or bone marrow-derived dendritic cells were compared in an in vitro infection assay. Immature dendritic cells such as Langerhans cells or bone marrow-derived dendritic cells were infected 10- to 30-fold more efficiently than mature splenic dendritic cells. Bone marrow-derived dendritic cells carrying an endogenous mouse Mammary Tumor virus superantigen were highly efficient at inducing a superantigen response in vivo. These results highlight the importance of professional APC and efficient T cell priming for the establishment of a persistent infection by mouse Mammary Tumor virus.
