The Neuro-Psychological Axis of Pancreatic Cancer as a Novel Target for Intervention

Abstract

phosphate (IP 3) and Diacylglycerol (DAG), thereby increasing intracellular Ca 2+ [17] (Figures 1 and 2). The α2-AR is coupled to the inhibitory G-protein Gi that inhibits the formation of intracellular cAMP by inactivating adenylyl cyclase [17] (Figure 2). All three known β-ARs (β1-β3) are coupled to the stimulatory G-protein G s while the β2-AR

Beta-Blocker Drug Use and Survival among Patients with Pancreatic Adenocarcinoma

“…The inconsistency of results between and within cancer types could be due to not only heterogeneity in tumor biology, but also methodological variations, including differences in exposure definitions and population selection. There may also be influences of variation in type and duration (10,45) of b-blocker use in earlier studies.…”

“…Beta-Blocker Drug Use and Survival among Patients with Updated version 10.1158/0008-5472.CAN-17-0108 doi:…”

“…SNS activation elevates catecholamine levels released systemically from the adrenal glands (8) and locally from postganglionic sympathetic nerve fiber termini, including in the pancreas (5). This neurotransmitter secretion is influenced not only by stress but also by other factors including smoking, diabetes mellitus, chronic pancreatitis, alcohol consumption, obesity, and hypertension (9)(10)(11).…”

Autophagy-Related Gene Expression Changes Are Found in Pancreatic Cancer and Neurodegenerative Diseases

“…The role of neurology genes in the progression and metastasis of cancer in general has been emphasized recently. In many reviews, Hildegard M. Schuller established the theory that modulation of the autonomic nervous system is responsible for driving cancer development, progression, and resistance to chemotherapy not only in non-small-cell lung cancer and pancreatic ductal adenocarcinoma but also in other cancers [43][44][45][46][47][48].…”

“…She anticipated the different modifiable risk factors of PDAC development, including smoking, chronic psychological stress, and habitual ingestion of alcohol, to act mostly via the sensitization (α7nAChR) and desensitization (α4nAChR) of nAChRs that drive the expression of proteins, which regulate the synthesis and release of catecholamines and GABA and result in the hyperactivity of Gs-mediated cAMP signaling [47]. α7nAChR activation is responsible for the production of stress neurotransmitters, which are known to promote cancer features, as well as of serotonin, dopamine, and glutamate, while the desensitization of α4nAChR is the main reason for reduced GABA levels, which is known to be a protective neurotransmitter [45].…”