Abstract
Background: Recent studies using mouse model of ovarian carcinoma have shown that chronic stress may influence tumor growth and angiogenesis by modulating the expression of matrix metalloproteinases (MMP) and vascular endothelial growth factor (VEGF) through the &bgr;-adrenergic receptor (&bgr;-AR)–cyclic AMP (cAMP)–protein kinase A (PKA) pathway. Our previous in vitro experiment data described that HIF-1&agr; as regulatory hinge mediated &bgr;-AR signaling pathway. The purpose of this study was to test the hypothesis that chronic stress in a negative social and psychological state plays a critical role in pancreatic cancer development and progression.
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