Heptamethoxyflavone Reduces Phosphodiesterase Activity and T-Cell Growth in vitro

2017 ◽  
Vol 174 (3-4) ◽  
pp. 113-120 ◽  
Author(s):  
Yui Hamada ◽  
Mitsunari Nakajima ◽  
Kazuna Tsuzuki ◽  
Yoshiaki Amakura ◽  
Morio Yoshimura ◽  
...  
1997 ◽  
Vol 43 (6) ◽  
pp. 345-354 ◽  
Author(s):  
T. D. Nguyen ◽  
Melanie J. Smith ◽  
Peter Hersey

Cytokine ◽  
1995 ◽  
Vol 7 (4) ◽  
pp. 355-363 ◽  
Author(s):  
Graham Pawelec ◽  
Heike Pohla ◽  
Elke Schlotz ◽  
Arnika Rehbein ◽  
Kurt Schaudt ◽  
...  

Blood ◽  
2006 ◽  
Vol 109 (6) ◽  
pp. 2496-2504 ◽  
Author(s):  
Laura Conti ◽  
Gabriella Regis ◽  
Angela Longo ◽  
Paola Bernabei ◽  
Roberto Chiarle ◽  
...  

Abstract Several approaches to target insulin-like growth factor-1 (IGF-1) signaling have resulted in the inhibition of the growth of a broad range of tumor cells. Malignant T cells are insensitive to the antiproliferative effects of the interferon-γ (IFN-γ)/signal transducer and activator of transcription 1 (STAT1) pathway because of the IGF-1–dependent internalization of the IFN-γR2 signaling chain. Here we show that human malignant T cells are also resistant to the growth inhibitory effect of both the IGF-1 receptor–specific inhibitor picropodophyllin (PPP) and retrovirus-mediated gene transfer of a dominant negative IGF-1 receptor. However, blockade of IGF-1 receptor perturbs IFN-γR2 internalization and induces its cell surface accumulation in malignant T cells. This allows the reinstatement of the IFN-γ–induced STAT1 activation, a high expression of proapoptotic molecules, and the suppression of malignant T-cell growth both in vitro and in vivo in a severe combined immunodeficiency (SCID) mouse model. These data indicate that the inhibition of IGF-1 signaling combined with IFN-γ administration could be a promising approach to suppress the growth of neoplastic T cells resistant to each treatment on its own.


1984 ◽  
Vol 131 (1) ◽  
pp. 183-183
Author(s):  
E. Kedar ◽  
B.L. Ikejiri ◽  
T. Timonen ◽  
G.D. Bonnard ◽  
J. Reid ◽  
...  

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