Special Issue "Targeted Intervention for Pancreatic Cancer Associated with Smoking, Alcohol Abuse and Psychological Stress"
A special issue of Cancers (ISSN 2072-6694).
Deadline for manuscript submissions: closed (30 April 2015)
Prof. Dr. Hildegard M. Schuller
Experimental Oncology Laboratory, Department of Biomedical and Diagnostic Sciences, College of Veterinary Medicine, University of Tennessee, 2407 River Drive, Knoxville, TN 37996, USA
Website | E-Mail
Interests: lung cancer; pancreatic cancer; neurotransmitters as regulators of cancer; effects of nicotine and tobacco-specific nitrosamines ion cancer; effects of psychological factors on cancer
Pancreatic cancer is the fourth leading cause of cancer deaths with a mortality near 100% within 2 years of diagnosis. Neither cancer prevention efforts nor advances in cancer therapy have improved the prognosis of this disease and the incidence of pancreatic cancer is even rising.
Smoking and alcoholism are established risk factors, while evidence for psychological stress as an additional risk factor has emerged more recently. Tobacco-specific carcinogenic nitrosamines cause activating point mutations in K-ras and inactivating mutations in the tumor suppressor gene p53, with both mutations frequently expressed in pancreatic cancer. In addition, these nitrosamines interfere with the autonomic regulation of cell and organ functions by the nervous system, thus compromising its important role in maintaining homeostasis. Both smoking and alcoholism can additionally cause pancreatitis, an independent additional risk factor for pancreatic cancer. A potential etiological link between pancreatic cancer and psychological stress has been suggested by preclinical data generated by two independent laboratories: chronic social stress significantly promoted the growth of pancreatic cancer xenografts in mice via the stress neurotransmitter-induced activation of multiple cellular pathways downstream of beta-adrenergic receptors and chronic treatment of mice with the stress neurotransmitter epinephrine caused p53 suppression via beta-adrenergic receptor signaling.
For this Special Issue of Cancers, we invite contributions that focus on mechanisms: how smoking, alcoholism, and psychological stress may contribute to the development and progression of pancreatic cancer and how the targeting of such mechanisms can be exploited to improve pancreatic cancer prevention and therapy.
Prof. Dr. Hildegard M. Schuller
Manuscript Submission Information
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access monthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.
- pancreatic cancer
- nicotinic receptor signaling
- G-protein-coupled receptor signaling
- cancer prevention
- cancer therapy
- psychological stress