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In a groundbreaking study, scientists from Cold Spring Harbor Laboratory (CSHL) in the US have unveiled a startling connection between chronic stress and the spread of cancer. Their findings, published in the journal Cancer Cell, shed light on how stress can exacerbate cancer metastasis, offering potential avenues for novel treatment strategies.

Chronic stress, a pervasive condition linked to increased risks of heart disease and strokes, has long been suspected to play a role in cancer progression. However, the precise mechanisms underlying this phenomenon have remained elusive until now. Researchers at CSHL have uncovered a pivotal link between stress and the formation of web-like structures called NETs (neutrophil extracellular traps) by white blood cells known as neutrophils.

Lead researcher Xue-Yan He, formerly of CSHL, emphasized the significance of understanding stress’s impact on cancer patients. “Stress is something we cannot really avoid in cancer patients,” said He. “It’s very important to understand how stress works on us.”

The research team simulated chronic stress in mice with cancer, observing a dramatic increase in metastasis after exposure to stress. This increase, up to fourfold in some cases, pointed to a clear association between stress and cancer spread.

Further investigation revealed that stress hormones called glucocorticoids triggered the formation of NETs by neutrophils. These NETs, typically deployed by the immune system to combat pathogens, created an environment conducive to cancer metastasis. Importantly, the team demonstrated that blocking NET formation or neutrophil response to glucocorticoids halted the stress-induced increase in metastasis, offering a potential avenue for intervention.

“It’s almost preparing your tissue for getting cancer,” explained Mikala Egeblad, Adjunct Professor at CSHL, highlighting the profound impact of chronic stress on cancer progression.

Professor Linda Van Aelst, also of CSHL, stressed the importance of integrating stress reduction into cancer treatment and prevention strategies. “Reducing stress should be a component of cancer treatment and prevention,” emphasized Van Aelst.

The implications of this research extend beyond cancer patients, with potential applications in preventive medicine and therapy development. By targeting the mechanisms linking chronic stress to cancer spread, future treatments could offer hope for patients by slowing or stopping metastasis before it takes hold.

The study represents a significant step forward in our understanding of the complex interplay between stress and cancer, paving the way for innovative approaches to tackling this deadly disease.

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