Sign up for Table of Contents Alerts.
Email this page
Print this page
Journal Club
VAV1: A New Target in Pancreatic Cancer?
Gina DeNicola and David A. Tuveson
volume 4 | issue 5
may 2005Pages: 509-511
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.
Pancreatic ductal adenocarcinoma (PDA) is arguably the most lethal malignancy in the United States. Despite the identification of many molecular alterations in PDA, this information has not translated into effective therapeutic strategies to date. A recent report in Cancer Cell (Fernandez-Zapico et al., Cancer Cell 2005, 7:39-49) reveals an unexpected role for the hematopoietic-specific RhoGEF VAV1 in pancreatic tumorigenesis, where ectopic expression of VAV1 as a result of promoter demethylation was identified in the majority of established cell lines and PDA tissue samples. Importantly, VAV1 expression was functionally required for optimal proliferation, transformation and survival of pancreatic cancer cell lines. This study provides the first evidence of VAV1 promoter demethylation as an event in cancer progression, suggesting that aberrant signaling pathways driven by VAV1 are potential therapeutic targets in PDA.
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.





