Next Article in Journal
Not All Next Generation Sequencing Diagnostics are Created Equal: Understanding the Nuances of Solid Tumor Assay Design for Somatic Mutation Detection
Next Article in Special Issue
The Role of nAChR and Calcium Signaling in Pancreatic Cancer Initiation and Progression
Previous Article in Journal
Targeting Protein Kinase C Downstream of Growth Factor and Adhesion Signalling
Previous Article in Special Issue
Targeting NK-1 Receptors to Prevent and Treat Pancreatic Cancer: a New Therapeutic Approach
Open AccessReview

Neural Regulation of Pancreatic Cancer: A Novel Target for Intervention

Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, Victoria 3052, Australia
Department of Visceral Surgery and Medicine, University Hospital Bern, Bern 3010, Switzerland
Department of Pathology, University of Melbourne, Parkville 3010, Australia
Cousins Center for PNI, UCLA Semel Institute, Jonsson Comprehensive Cancer Center, and UCLA AIDS Institute, University of California Los Angeles, Los Angeles, CA 90095, USA
Peter MacCallum Cancer Centre, Division of Cancer Surgery, East Melbourne, Victoria 3002, Australia
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Academic Editor: Hildegard M. Schuller
Cancers 2015, 7(3), 1292-1312;
Received: 5 June 2015 / Revised: 7 July 2015 / Accepted: 13 July 2015 / Published: 17 July 2015
The tumor microenvironment is known to play a pivotal role in driving cancer progression and governing response to therapy. This is of significance in pancreatic cancer where the unique pancreatic tumor microenvironment, characterized by its pronounced desmoplasia and fibrosis, drives early stages of tumor progression and dissemination, and contributes to its associated low survival rates. Several molecular factors that regulate interactions between pancreatic tumors and their surrounding stroma are beginning to be identified. Yet broader physiological factors that influence these interactions remain unclear. Here, we discuss a series of preclinical and mechanistic studies that highlight the important role chronic stress plays as a physiological regulator of neural-tumor interactions in driving the progression of pancreatic cancer. These studies propose several approaches to target stress signaling via the β-adrenergic signaling pathway in order to slow pancreatic tumor growth and metastasis. They also provide evidence to support the use of β-blockers as a novel therapeutic intervention to complement current clinical strategies to improve cancer outcome in patients with pancreatic cancer. View Full-Text
Keywords: pancreatic cancer; beta-adrenergic; stress; beta-blockers; neural; metastasis pancreatic cancer; beta-adrenergic; stress; beta-blockers; neural; metastasis
Show Figures

Figure 1

MDPI and ACS Style

Chang, A.; Kim-Fuchs, C.; Le, C.P.; Hollande, F.; Sloan, E.K. Neural Regulation of Pancreatic Cancer: A Novel Target for Intervention. Cancers 2015, 7, 1292-1312.

Show more citation formats Show less citations formats

Article Access Map by Country/Region

Only visits after 24 November 2015 are recorded.
Search more from Scilit
Back to TopTop