scholarly journals Combination of tumor necrosis factor-? with sulindac augments its apoptotic potential and suppresses tumor growth of human carcinoma cells in nude mice

Cancer ◽  
2003 ◽  
Vol 97 (6) ◽  
pp. 1412-1420 ◽  
Author(s):  
Hiroshi Yasui ◽  
Masaaki Adachi ◽  
Kohzoh Imai
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Growth ◽  
Nude Mice ◽  
Tumor Necrosis ◽  
Carcinoma Cells ◽  
Human Carcinoma ◽  
Necrosis Factor

Soluble Tumor Necrosis Factor-Like Weak Inducer of Apoptosis Overexpression in HEK293 Cells Promotes Tumor Growth and Angiogenesis in Athymic Nude Mice

2004 ◽  
Vol 64 (24) ◽  
pp. 8968-8972 ◽  
Author(s):  
David H. Ho ◽  
Hong Vu ◽  
Sharron A. N. Brown ◽  
Patrick J. Donohue ◽  
Heather N. Hanscom ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Growth ◽  
Nude Mice ◽  
Tumor Necrosis ◽  
Hek293 Cells ◽  
Athymic Nude Mice ◽  
Necrosis Factor

scholarly journals Chronic exposure to tumor necrosis factor in vivo preferentially inhibits erythropoiesis in nude mice

Blood ◽  
1989 ◽  
Vol 74 (1) ◽  
pp. 130-138 ◽  
Author(s):  
RA Johnson ◽  
TA Waddelow ◽  
J Caro ◽  
A Oliff ◽  
GD Roodman
Keyword(s):  
Tumor Necrosis Factor ◽  
Nude Mice ◽  
Tumor Necrosis ◽  
Chinese Hamster ◽  
Anemia Of Chronic Disease ◽  
Produce Tumor Necrosis Factor ◽  
Tnf Gene ◽  
Necrosis Factor

Abstract The anemia of chronic disease (ACD) is associated with conditions in which macrophage activation occurs. Activated marrow macrophages suppress erythropoiesis in vitro and produce tumor necrosis factor (TNF). Therefore, we tested the effects of chronic in vivo exposure to TNF to determine if it was a candidate for a mediator of ACD. Nude mice were inoculated with Chinese hamster ovary (CHO) cells expressing the human TNF gene or with control cells containing the transfection vector alone. The TNF mice promptly became reticulocytopenic, and after 3 weeks their corrected reticulocytes were 2.6% +/- 0.7% as compared with 7.3% +/- 4% in control mice. The hematocrit at 3 weeks was 28.4% +/- 1.7% in TNF mice as compared with 46% +/- 0.8% in control mice. This anemia was also associated with low serum iron and normal iron stores and increased erythropoietin (Epo) levels. The TNF mice showed an absolute monocytosis with twice the number of circulating monocytes as control mice and had M-colony-stimulating factor (CSF) activity in their serum. The TNF mice also became mildly thrombocytopenic. Marrow CFU-E and BFU-E were profoundly decreased (1.2 +/- 0.2 x 10(3) v 8.6 +/- 0.2 x 10(4) CFU-E per femur, and 6.5 +/- 1 x 10(2) v 8.5 +/- 0.2 x 10(4) BFU-E per femur). Splenic CFU-E and BFU-E were similarly depressed. In contrast, marrow CFU-GM and CFU-GEMM were not affected. The residual BFU-E in TNF mice were relatively resistant to TNF as compared with control mice. These data demonstrate that TNF preferentially inhibits erythropoiesis in vivo and may be important in the pathogenesis of ACD.

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