2014 Grant Recipient Daphna Bar-Sagi, PhD

Home Research Research Grants Program Grants Awarded Grants Awarded by Year 2014 Pancreatic Cancer Action Network Research Grants 2014 Grant Recipient Daphna Bar-Sagi, PhD

GRANTEE: Dafna Bar-Sagi, PhD
Institution: New York University School of Medicine
Research Project: PDA development: Heads or tails?
Award: 2014 Pancreatic Cancer Action Network – AACR Innovative Grant
Award Period: July 1, 2014 – June 30, 2016
Amount: $200,000

Click here to download Dr. Bar-Sagi’s 2014 Grant Snapshot (pdf)

Institution: New York University School of Medicine
Research Project: Impact of Diet-Induced Hyperlipidemia on Pancreatic Inflammation
and Cancer
Award: 2008 Pancreatic Cancer Action Network – AACR Pilot Grant
Award Period: July 1, 2008 – June 30, 2010
Amount: $100,000

Click here to download Dr. Bar-Sagi’s 2008 Grant Snapshot (pdf)

Biographical Highlights
Dr. Bar-Sagi is a Professor in the Department of Medicine and the Department of Biochemistry and Molecular Pharmacology, Senior Vice President and Vice Dean for Science, and Chief Scientific Officer at New York University Langone Medical Center. Prior to this she was Chair of the Department of Biochemistry at New York University Langone Medical Center following a Chair position in the Department of Microbiology and Molecular Genetics at SUNY Stony Brook. This is Dr. Bar-Sagi’s third research grant from the Pancreatic Cancer Action Network; she is the co-principal investigator on the 2013 Tempur-Pedic – Inaugural Research Acceleration Network Grant in memory of Tim Miller, and received a Pilot Grant in 2008. In addition, several postdoctoral trainees of Dr. Bar-Sagi have received grants from the organization. Dr. Bar-Sagi is also a member of the Scientific and Medical Advisory Board.

She is a world authority in the field of oncogenic signaling and has made fundamental contributions to the understanding of the role of Ras oncogenes in tumor development. She has devoted the past decade to demystifying the complex functions of the Ras oncogene in pancreatic cancer, an effort that has led to the identification of specific effector mechanisms that are critical for the tumorigenic process, including inflammation, immunity and metabolism.

2014 Project Overview
The pancreas is an elongated soft gland divided into three sections: the head, the body and the tail. A well-documented but poorly understood and understudied clinical aspect of pancreatic cancer is that in the majority of patients (close to 80 percent), the tumors develop in the head rather than the tail of the pancreas, indicating that the anatomical location within the pancreas can dictate the course of tumor development (also known as tumorigenesis). However, the mechanisms underlying this region-specific difference in tumorigenic potential are unknown, and their identification is the major goal of the studies outlined by Dr. Bar-Sagi in this proposal.

Specifically, Dr. Bar-Sagi and her colleagues will employ diverse strategies to pursue two specific aims: (1) to characterize the differential capacity of precancerous pancreatic abnormalities to develop and progress in the head and the tail of the pancreas, and (2) to identify determinants outside of the cell that confer distinct precancerous growth properties in the head and the tail of the pancreas. These efforts will improve our biological understanding of the drivers of pancreatic tumorigenesis and, as such, should provide novel insights into the eventual design of effective therapeutic strategies for this disease.


2008 Project Overview
The funded project focuses on the relationship between high fat diet-induced hyperlipidemia and the development of pancreatic cancer. Hyperlipidemia is an excess of fatty substances called lipids, largely cholesterol and triglycerides, in the blood. High fat diet and obesity have been implicated in the etiology of chronic pancreatitis (inflammation of the pancreas) and pancreatic cancer. However, the mechanistic basis of this association remains unknown. The overall goal of the project is to establish a mouse model and investigate this link. The experimental design will take advantage of mice that have been genetically engineered to develop hyperlipidemia following feeding of a high fat diet. These mice will be employed to (1) characterize the structural changes that the pancreas endures in response to hyperlipidemia; and (2) assess the effects of hyperlipidemia on pancreatic cancer development. By exploring the cause-and-effect relationships between hyperlipidemia and pancreatic carcinogenesis, these studies will provide new insights into the epidemiological connection between obesity, high fat diet and pancreatic cancer.

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