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Specific Tumor Suppressor Function for E2F2 in Myc-Induced T Cell Lymphomagenesis

Deregulation of the Myc pathway and deregulation of the Rb pathway are two of the most common abnormalities in human malignancies. Recent in vitro experiments suggest a complex cross-regulatory relationship between Myc and Rb that is mediated through the control of E2F. To evaluate the functional co... Full description

Main Author: Opavsky, Rene
Contributors: Tasi, Shih-Yin | Author
Guimond, Martin | Author
Arora, Anjulie | Author
Opavska, Jana | Author
Becknell, Brian | Author
Kaufmann, Michael | Author
Walton, Nathaniel A. | Author
Stephens, Julie A. | Author
Fernandez, Soledad A. | Author
Muthusamy, Natarajan | Author
Felsher, Dean W. | Author
Porcu, Pierluigi | Author
Caligiuri, Michael A. | Author
Leone, Gustavo | Author
Contained in: Proceedings of the National Academy of Sciences of the United States of America Washington, DC : National Acad. of Sciences Vol. 104, No. 39 (2007), p. 15400-15405
Journal Title: Proceedings of the National Academy of Sciences of the United States of America
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Links: Volltext (www.jstor.org)
ISSN: 0027-8424
Additional Keywords: Cancer
Transcription
research-article
Language: English
Notes: Copyright: Copyright 2007 The National Academy of Sciences of the United States of America
Physical Description: Online-Ressource
ID (e.g. DOI, URN): 25449147
10.1073/pnas.0706307104
PPN (Catalogue-ID): JST070113521
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520 |a Deregulation of the Myc pathway and deregulation of the Rb pathway are two of the most common abnormalities in human malignancies. Recent in vitro experiments suggest a complex cross-regulatory relationship between Myc and Rb that is mediated through the control of E2F. To evaluate the functional connection between Myc and E2Fs in vivo, we used a bitransgenic mouse model of Myc-induced T cell lymphomagenesis and analyzed tumor progression in mice deficient for E2f1, E2f2, or E2f3. Whereas the targeted inactivation of E2f1 or E2f3 had no significant effect on tumor progression, loss of E2f2 accelerated lymphomagenesis. Interestingly, loss of a single copy of E2f2 also accelerated tumorigenesis, albeit to a lesser extent, suggesting a haploinsufficient function for this locus. The combined ablation of E2f1 or E2f3, along with E2f2, did not further accelerate tumorigenesis. Mycoverexpressing T cells were more resistant to apoptosis in the absence of E2f2, and the reintroduction of E2F2 into these tumor cells resulted in an increase of apoptosis and inhibition of tumorigenesis. These results identify the E2f2 locus as a tumor suppressor through its ability to modulate apoptosis. 
653 |a research-article 
653 |a Transcription 
653 |a Cancer 
700 1 |a Tasi, Shih-Yin  |e verfasserin  |4 aut 
700 1 |a Guimond, Martin  |e verfasserin  |4 aut 
700 1 |a Arora, Anjulie  |e verfasserin  |4 aut 
700 1 |a Opavska, Jana  |e verfasserin  |4 aut 
700 1 |a Becknell, Brian  |e verfasserin  |4 aut 
700 1 |a Kaufmann, Michael  |e verfasserin  |4 aut 
700 1 |a Walton, Nathaniel A.  |e verfasserin  |4 aut 
700 1 |a Stephens, Julie A.  |e verfasserin  |4 aut 
700 1 |a Fernandez, Soledad A.  |e verfasserin  |4 aut 
700 1 |a Muthusamy, Natarajan  |e verfasserin  |4 aut 
700 1 |a Felsher, Dean W.  |e verfasserin  |4 aut 
700 1 |a Porcu, Pierluigi  |e verfasserin  |4 aut 
700 1 |a Caligiuri, Michael A.  |e verfasserin  |4 aut 
700 1 |a Leone, Gustavo  |e verfasserin  |4 aut 
773 0 8 |i in  |t Proceedings of the National Academy of Sciences of the United States of America  |d Washington, DC : National Acad. of Sciences  |g Vol. 104, No. 39 (2007), p. 15400-15405  |q 104:39<15400-15405  |w (DE-601)JST069399220  |x 0027-8424 
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