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Impact of Chronic Stress and Diet on Pancreatic Cancer Development

Recent research conducted by investigators at UCLA has uncovered that continuous stress combined with poor dietary choices may accelerate the early onset of pancreatic cancer, highlighting the significant role that lifestyle factors play in this aggressive disease.

The study utilized preclinical models to reveal a crucial molecular mechanism whereby stress and obesity induce changes in pancreatic cells that could lead to tumor formation. Researchers discovered that stress-related neurotransmitters and hormones associated with obesity have the ability to activate a protein known as CREB, which is implicated in cancer cell proliferation. This activation occurs through distinct biological pathways: the stress hormones engage the β-adrenergic receptor/PKA pathway, while elements linked to obesity primarily utilize the PKD pathway. This indicates a shared mechanism through which both stress and obesity can propel the advancement of pancreatic cancer.

During experiments on mice, the administration of a high-fat diet was linked to the emergence of precancerous pancreatic lesions. Notably, the presence of social isolation stress in these mice led to the development of more advanced lesions, suggesting a compounded effect of diet and social stress on cancer progression.

The research also indicated that female mice exhibited a more pronounced reaction to social isolation in terms of cancer development compared to their male counterparts. The authors propose that biological differences in stress response, potentially influenced by estrogen and heightened activity of β-adrenergic receptors, might render females more vulnerable to stress-related cancer risks.

These findings underscore the potential of stress and obesity-related hormones in triggering key pathways that promote cancer, possibly hastening the progression of pancreatic cancer. In light of these results, the researchers propose investigating the potential of existing medications to reduce such risks. Specifically, as β-adrenergic receptors are vital in the context of stress-indicated cancer growth, beta-blockers—medications frequently prescribed for hypertension—could be considered for repurposing to help alleviate these effects.

This study received funding from notable institutions including the National Cancer Institute, the National Institute of Allergy and Infectious Diseases, along with support from the Ronald S. Hirshberg Endowed Chair of Pancreatic Cancer Research and the Ronald S. Hirshberg Foundation.

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