Title:
Molecular Approaches to Diet and Pancreatic Cancer Prevention (R01) (PA)

Contact:

Sharon A. Ross, PhD, MPH
Nutritional Science Research Group
Division of Cancer Prevention
NCI, NIH, DHHS
6130 Executive Boulevard, Room 3157
Bethesda, MD 20892-7328
Telephone: 301-594-7547
Fax: 301-480-3925
Email: rosssha@mail.nih.gov

Objective of Project:

The purpose of this initiative is to invite innovative preclinical and clinical R01 applications to determine how the dietary intake of energy and bioactive food components influence pancreatic cancer development and prevention. This Program Announcement (PA) seeks to encourage collaboration between nutritional scientists and cancer biologists/oncologists and gastroenterologists to jointly examine key mechanisms in the pancreatic cancer process (i.e., carcinogen metabolism, cell division, differentiation, apoptosis) in order to begin to establish mechanistic links between quantity and form of energy consumed and/or bioactive food component intakes with pancreatic tumor incidence/behavior.

Description of Project:

Approximately 30,000 Americans are diagnosed yearly with pancreatic cancer. This is a particularly devastating cancer since the case-fatality proportion approaches 90 percent within twelve months following diagnosis, making prevention approaches important. It is widely acknowledged that genetic, epigenetic, and environmental factors influence the onset of pancreatic cancer. The linkage between diet and pancreatic cancer comes from its longstanding recognized interrelationship with diabetes and obesity, and thus caloric intake and expenditure. This PA seeks to expand research that will clarify the importance of diet-induced energetics and bioactive food components in pancreatic cancer prevention. Specifically, preclinical and clinical studies are sought that utilize innovative molecular biological approaches to determine the importance of energy intake and/or bioactive food constituents as site specific modifiers of the pancreatic cancer process. Some of the possible mechanistic pathways leading to pancreatic cancer involve: insulin signaling pathways (e.g., insulin-like growth factors [IGF]), the impact of glycated proteins, free radical damage, and aberrant methylation processes. The discovery, identification, and characterization of the role of dietary components in regulating these and other processes in the development of pancreatic cancer deserves further study, and serves as the basis of this PA.