Viewpoints / Position Papers
Factors connecting inflammation to pancreatic cancer initiation and progression
Dual grant recipient Matthias Hebrok, PhD (2008 Michael C. Sandler -- Pancreatic Cancer Action Network – AACR Pilot Grant and 2011 Abby Sobrato -- Pancreatic Cancer Action Network -- AACR Innovative Grant) published a pivotal study in the prestigious journal Cancer Cell on April 12, 2011. Dr. Hebrok’s 2008 Pancreatic Cancer Action Network grant is cited as a funding source for the work published in this article; his 2011 funding period will begin in July.
Dr. Hebrok’s laboratory is at the University of California, San Francisco. Additional collaborating authors on this study are located at Osaka University in Japan, and the University of Utah. Dr. Hebrok and colleagues sought to better understand the relationship between inflammation and the development of pancreatic cancer. Chronic pancreatitis, or constant inflammation of the pancreas, has previously been labeled as a risk factor for pancreatic cancer. However, the molecular mechanism of this relationship had not been defined. Here, the researchers determined that two proteins, Stat3 and MMP7, contribute directly to inflammation-related pancreatic cancer initiation and metastasis (spread), respectively.
A potential clinical implication of this study is that both proteins may be therapeutically targetable in pancreatic cancer patients. Specifically, the authors discuss inhibition of Stat3 and/or MMP7 immediately following surgery, to block further progression of the disease. Additionally, analyses of serum (a component of blood) samples of pancreatic cancer patients revealed that the protein MMP7 is measurable in serum, and higher MMP7 levels correlated with a worse prognosis. Knowledge of which individuals may best benefit from certain treatments could greatly improve the outcome for pancreatic cancer patients.
For more information about this study or other questions about pancreatic cancer risk factors, diagnosis, or treatment, please contact a Pancreatic Cancer Action Network PALS Associate toll-free at 877-272-6226 or email email@example.com. PALS Associates are available M-F 7am-5pm Pacific Time.
Click here for the scientific abstract of the paper.
Click here for the UCSF press release.