In this issue of The Journal of Experimental Medicine, Hudson et al. 1 report on the identification of a cytokine, the macrophage migration inhibitory factor or MIF, that overcomes p53 function by suppressing its transcriptional activity, thus linking complex programs that govern proinflammatory response and cell fate. p53 has a key role in the regulation of cell growth and death, and its involvement in these regulatory systems may reflect its ability to respond to different cellular stress situations by inducing cell cycle arrest or apoptosis (see references 2–4 for reviews on the topic and below for more details on p53 function). When altered by germ line or somatic mutations, by aberrant patterns of expression, or through the inactivating potential of Mdm2 or certain viral oncoproteins, loss of wild-type p53 function is responsible for tumorigenesis and tumor progression 5...
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15 November 1999
Commentary|
November 15 1999
At the Crossroads of Inflammation and Tumorigenesis
Carlos Cordon-Cardo,
Carlos Cordon-Cardo
aDepartment of Pathology, Memorial Sloan-Kettering Cancer Center, New York, New York 10021
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Carol Prives
Carol Prives
bDepartment of Biological Sciences, Columbia University, New York, New York 10027
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Carlos Cordon-Cardo
aDepartment of Pathology, Memorial Sloan-Kettering Cancer Center, New York, New York 10021
Carol Prives
bDepartment of Biological Sciences, Columbia University, New York, New York 10027
Received:
September 13 1999
Accepted:
September 28 1999
Online ISSN: 1540-9538
Print ISSN: 0022-1007
© 1999 The Rockefeller University Press
1999
The Rockefeller University Press
J Exp Med (1999) 190 (10): 1367–1370.
Article history
Received:
September 13 1999
Accepted:
September 28 1999
Citation
Carlos Cordon-Cardo, Carol Prives; At the Crossroads of Inflammation and Tumorigenesis. J Exp Med 15 November 1999; 190 (10): 1367–1370. doi: https://doi.org/10.1084/jem.190.10.1367
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