Inhibition of NF-kappaB enhances the anti-tumor effect of combination treatment with tumor necrosis factor-alpha (TNF-alpha) gene therapy and gemcitabine for pancreatic cancer in mice

2012 ◽  
Vol 215 (3) ◽  
pp. S24
Author(s):  
Yuki Fujiwara ◽  
Hiroaki Shiba ◽  
Ryota Iwase ◽  
Koichiro Haruki ◽  
Kenei Furukawa ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Gene Therapy ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Alpha Gene ◽  
Nf Kappab ◽  
Necrosis Factor

scholarly journals 2-Aminopurine selectively inhibits splicing of tumor necrosis factor alpha mRNA.

1996 ◽  
Vol 16 (6) ◽  
pp. 2814-2822 ◽  
Author(s):  
N Jarrous ◽  
F Osman ◽  
R Kaempfer
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Translation Initiation Factor ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Rnase Protection ◽  
Factor Alpha ◽  
Alpha Gene ◽  
Necrosis Factor

2-Aminopurine (2-AP) inhibits specific kinases that phosphorylate the alpha subunit of eukaryotic translation initiation factor 2. One of these, PKR, is also involved in signal transduction. We show here that 2-AP selectively inhibits expression of tumor necrosis factor alpha (TNF-alpha) mRNA in primary human lymphoid cells. 2-AP does not inhibit transcription of the human TNF-alpha gene, nor does it affect mRNA stability. Instead, the flow of short-lived precursor transcripts into mature TNF-alpha mRNA is blocked. When 2-AP is present during induction, unspliced TNF-alpha precursor transcripts accumulate at the expense of mRNA. Using RNase protection analysis with genomic probes for different exon-intron junctions, we show that 2-AP blocks splicing of TNF-alpha mRNA. Neither the TNF-beta nor the interleukin-1 beta gene shows such regulation. 2-AP also inhibits splicing of precursor RNA transcribed from an exogenous human TNF-alpha gene. Sequences within this gene thus confer sensitivity to 2-AP. Yet, control is not exerted at a specific splice site. Our results reveal the involvement of a 2-AP-sensitive component, expressed in functional form before induction, in the splicing of TNF-alpha mRNA.

Resection of pancreatic cancer normalizes the preoperative increase of tumor necrosis factor alpha gene expression

Pancreatology ◽  
2002 ◽  
Vol 2 (5) ◽  
pp. 491-494 ◽  
Author(s):  
Parisa Ariapart ◽  
Susanne Bergstedt-Lindqvist ◽  
Vanessa van Harmelen ◽  
Johan Permert ◽  
Feng Wang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pancreatic Cancer ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Alpha Gene ◽  
Necrosis Factor

scholarly journals Alleles 308A and 238A in the Tumor Necrosis Factor Alpha Gene Promoter Do Not Increase the Risk of Severe Malaria in Children with Plasmodium falciparum Infection in Mali

2006 ◽  
Vol 74 (12) ◽  
pp. 7040-7042 ◽  
Author(s):  
Sandrine Cabantous ◽  
Ogobara Doumbo ◽  
Stéphane Ranque ◽  
Belco Poudiougou ◽  
Abdoulaye Traore ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Severe Malaria ◽  
Tumor Necrosis ◽  
Gene Promoter ◽  
Falciparum Infection ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Alpha Gene ◽  
Necrosis Factor

ABSTRACT The hypothesis that tumor necrosis factor (TNF) aggravates malaria in children is supported by observations that TNF polymorphisms and high TNF levels have been associated with cerebral malaria. Nevertheless, severe malaria was not associated with polymorphisms located at positions −308A and −238A in the TNF alpha gene promoter or with a high TNF level in plasma in children from Bamako, Mali.

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