Rac1 GTPase in pancreatic cancer.

Ying Yan,Michel M Ouellette

doi:10.18632/aging.100804

Abstract

Rac1 GTPase in pancreatic cancer.

Highlights

Pancreatic cancer is the fourth leading cause of cancer death in the Western world
In mouse models of pancreatic cancer, the pancreas specific activation of K-Ras leads to acinar-to-ductal metaplasia (ADM) and formation of PanIN precursor lesions
Recent studies have used interfering RNA, pharmacological inhibitors, or dominant negative mutant of related C3 botulinum toxin substrate 1 (Rac1) (Rac1T17N) to block Rac1 signaling in cultivated pancreatic cancer cells

Summary

Introduction

Pancreatic cancer is the fourth leading cause of cancer death in the Western world. It is a disease of insidious progression and high lethality, with a 5 year survival rate of only 6%. Editorial have never been measured in pancreatic cancer specimens, the pathway is generally assumed to be activated in these tumors, at least in part by the presence of activated K-Ras. Recent studies have highlighted the role of Rac1 in the initiation and progression of pancreatic cancer. In mouse models of pancreatic cancer, the pancreas specific activation of K-Ras leads to acinar-to-ductal metaplasia (ADM) and formation of PanIN precursor lesions.

Results

Conclusion