Breaking the NF-κB and STAT3 alliance inhibits inflammation and pancreatic tumorigenesis.
This perspective on Liby et al. (beginning on page 1427 in this issue of the journal) discusses the importance of the finding that two synthetic triterpenoids prolonged survival in a pancreatic cancer mouse model. This finding is significant because pancreatic cancer is one of the deadliest human cancers. These compounds inhibited the interaction between NF-κB and signal transducer and activator of transcription 3, and determining the mechanisms underlying this inhibition will help to rapidly move these compounds into phase I clinical trials.
Surh
Young-Joon
YJ
The Hormel Institute, University of Minnesota, 801 16th Avenue Northeast, Austin, MN 55912-3679. zgdong@hi.umn.edu.
Bode
Ann M
AM
Dong
Zigang
Z
D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology*; D006801:Humans; D007249:Inflammation / Q000188:drug therapy* / Q000378:metabolism; D051379:Mice; D016328:NF-kappa B / Q000378:metabolism*; D010190:Pancreatic Neoplasms / Q000188:drug therapy* / Q000378:metabolism; D050796:STAT3 Transcription Factor / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects*
D000970:Antineoplastic Agents; D016328:NF-kappa B; D050796:STAT3 Transcription Factor