NF-kappaB in pancreatic cancer. Int J Gastrointest Cancer 2003;33(1):15-26
Date
08/12/2003Pubmed ID
12909735DOI
10.1385/IJGC:33:1:15Scopus ID
2-s2.0-1542678177 (requires institutional sign-in at Scopus site) 56 CitationsAbstract
Although the genetic profile of pancreatic cancer is emerging as a result of much research, the role of specific genetic alterations that initiate tumorigenesis and produce its cardinal clinical features of locally aggressive growth, metastasis, and chemotherapy resistance remains unresolved. Recently, a number of studies have shown that the inhibition of constitutive NF-kappaB activation, one of the frequent molecular alterations in pancreatic cancer, inhibits tumorigenesis and metastasis. It also sensitizes pancreatic cancer cell lines to anticancer agent-induced apoptosis. Therefore because of the crucial role of NF-kappaB in pancreatic cancer, it is a potential target for developing novel therapeutic strategies for the disease. In vivo and in vitro models that mimic the tumorigenic phenotypes in the appropriate histological and molecular concert would be very useful for confirming the suspected role of the pancreatic cancer signature genetic lesions and better understanding the molecular basis of this disease.
Author List
Sclabas GM, Fujioka S, Schmidt C, Evans DB, Chiao PJAuthor
Douglas B. Evans MD Chair, Professor in the Surgery department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsGene Expression Regulation, Neoplastic
Humans
NF-kappa B
Oncogenes
Pancreatic Neoplasms
Signal Transduction
