1. Molecular Pathology of Pancreatic Cancer: Implications for Molecular Targeting Therapy 
Toru Furukawa 
Clinical Gastroenterology and Hepatology 
Volume 7, Issue 11, Pages S35-S39 (November 2009)
DOI: /j.cgh
Copyright © 2009 AGA Institute Terms and Conditions

2. Figure 1
What is the origin of pancreatic cancer? (A) Acinar-ductal metaplasia. (B) Pancreatic intraepithelial neoplasia. (C) Ductal adenocarcinoma. Images were taken from human pancreas involved with ductal adenocarcinoma.
Clinical Gastroenterology and Hepatology 2009 7, S35-S39DOI: ( /j.cgh )
Copyright © 2009 AGA Institute Terms and Conditions

3. Figure 2
The RAS-MAPK pathway is implicated in malignant phenotypes of pancreatic cancer. Gain-of-function mutations in KRAS generate a protein that can be irreversibly activated by receptor tyrosine kinases (RTK) and that is refractory to suppression by upstream growth factors (GF). Activated RAS stimulates downstream signaling cascades including RAF1-MAP2K1-MAPK1. Epigenetic loss of function of DUSP6 synergistically contributes to constitutive activation of MAPK1 that induces activation of its downstream target molecules. The downstream targets of MAPK1 are central to the development of the malignant phenotypes and are candidates for therapeutic molecular targets of pancreatic cancer.
Clinical Gastroenterology and Hepatology 2009 7, S35-S39DOI: ( /j.cgh )
Copyright © 2009 AGA Institute Terms and Conditions