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NYU Dentistry and Medicine are awarded a $840,864 collaborative grant by the Lustgarten Foundation

New York University College of Dentistry (NYUCD) and New York University School of Medicine (SOM) researchers have been awarded a four-year $840,864 collaborative grant by the Lustgarten Foundation to investigate a potential link between pancreatic cancer development and endogenous gut microbiota.

The co-investigators, Deepak Saxena, MS, PhD, Assistant Professor, Basic Science and Craniofacial Biology at NYUCD, and George Miller, MD, Assistant Professor; Departments of Surgery and Cell Biology at the SOM, seek to explore the links between the intestinal microbiome, Toll-like receptors (TLRs), and pancreatic cancer.

"Endogenous gut microbiota have recently been appreciated as important regulators of homeostasis in the healthy individual and contributors toward disease during microbiotic imbalance," said Saxena. "The microbiome is also emerging as a contributor to carcinogenesis in extra-pancreatic malignancies such as colon and liver cancer. However, there has been no direct link between pancreatic cancer development and endogenous gut microbiota," he noted.

There are tangential data, however, that support such an association. For example, the oral microbiome in patients with pancreatic cancer has been found to substantially differ from control subjects. Preliminary data suggest that the intestinal microbiome may be an important regulator of pancreatic cancer development in at-risk individuals.

The study proposes to:

  • Define the evolving intestinal microbiome in mice during pancreatic cancer development and progression as well as determine whether humans with pancreatic cancer harbor a distinct microbiome compared with age-matched control patients

  • Directly test whether endoluminal bacteria can affect pancreatic oncogenesis and determine whether selectively modulating the microbiome alters the rate of tumor progression

  • Test the hypothesis that luminal pathogens affect pancreatic tumorigenesis specifically via TLR ligation

"Our experiments will provide critical new information on the mechanism of pancreatic carcinogenesis in at-risk hosts and, as such, will provide guidance for pancreatic cancer prevention and possibly treatment of incipient disease," said Saxena.

"Based on our past research, we postulate that specific pathogenic gut bacteria drive pancreatic carcinogenesis in at-risk individuals via TLR activation," said Miller.

As a part of their grant, Drs. Saxena and Miller will be attending and presenting at the annual Lustgarten Scientific Conference to be held October 20-22, 2013, at the Banbury Center on Long Island NY.


Contact: Christopher James
New York University

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