In a groundbreaking study conducted by researchers at Cold Spring Harbor Laboratory (CSHL), a profound connection between chronic stress and the spread of cancer has been unveiled.
Led by former CSHL postdoc Xue-Yan He, along with Adjunct Professor Mikala Egeblad and Professor Linda Van Aelst, the study sheds light on the mechanisms through which stress exacerbates cancer metastasis. Published in Cancer Cell, their findings open new avenues for potential treatment strategies to halt cancer progression before it gains momentum.
Stress, an unavoidable aspect of modern life, has long been recognized as a detriment to health, with links to heart disease, strokes, and now, cancer metastasis. The team embarked on their investigation to decipher the intricate relationship between stress and cancer spread, recognizing the pressing need for insights into this critical area of cancer care.
He, now an Assistant Professor of Cell Biology & Physiology at Washington University School of Medicine in St. Louis, highlights the significance of understanding how stress impacts cancer patients.
“Stress is something we cannot really avoid in cancer patients,” He explains. “You can imagine if you are diagnosed, you cannot stop thinking about the disease or insurance or family. So it is very important to understand how stress works on us.”
Research on Mice To Understand The Link Between Chronic Stress and Cancer
The researchers simulated chronic stress in mice with cancer, observing a startling increase in metastatic lesions in stressed mice compared to a control group. Egeblad recalls the dramatic findings, noting a fourfold increase in metastasis in stressed mice.
The team pinpointed the role of stress hormones, particularly glucocorticoids, in triggering the formation of sticky web-like structures called NETs (neutrophil extracellular traps) by certain white blood cells known as neutrophils.
NETs, typically involved in defending the body against microbial invaders, take on a sinister role in cancer by creating an environment conducive to metastasis. His experiments confirmed that stress-induced NET formation significantly contributed to increased metastasis.
Remarkably, chronic stress not only facilitated cancer spread but also primed lung tissue for potential cancer development, even in mice without cancer.
The implications of these findings are profound. Van Aelst emphasizes the importance of integrating stress reduction into cancer treatment and prevention strategies. “Reducing stress should be a component of cancer treatment and prevention,” she asserts.
Moreover, the team speculates that future drugs targeting NET formation could hold promise in slowing or halting cancer metastasis, offering much-needed relief for patients at risk of cancer spread.
The study represents a significant leap forward in understanding the complex interplay between stress and cancer progression. By elucidating the mechanisms through which stress fuels metastasis, the researchers have identified potential targets for intervention and underscored the importance of addressing stress in cancer care.
Moving forward, further research will be needed to explore the feasibility and efficacy of targeting NET formation as a therapeutic approach. Nevertheless, the study’s findings offer hope for the development of innovative treatments aimed at curbing cancer metastasis and improving patient outcomes.
In summary, the study conducted by CSHL researchers unveils a compelling link between chronic stress and cancer spread, paving the way for novel therapeutic strategies and highlighting the critical role of stress management in cancer care.
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