
Chronic periods of stress can be detrimental to health by increasing inflammation and promoting the progression of diseases including cancer.
A new study published in the Journal Nature Communications revealed that chronic stress can impact functioning of lymphatic system triggering cancer metastasis.
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‘Chronic stress remodels tumor-associated lymphatic architecture to promote lymph node metastasis.’
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The lymphatic system helps carry immune cells through the body to fight illness, but it could also play a role in transporting cancer cells through the body.
Researchers at the Melbourne's Monash University conducted a study on mice with cancer. They examined whether stress can influence cancer spread to other parts of the body.
They found that high levels of stress triggers the production of adrenaline by the activation of sympathetic nervous system (SNS) that causes large amount of fluids to enter into the lymphatic system. The entry of fluids causes the lymphatic system to expand, resulting in high fluid inflow and outflow.
The researchers describe this mechanism as "lymphatic highway" which influences the cancer cells to spread through the body. Adrenaline not only increases the number of lymphatic vessels draining from the tumor but also increase the flow in existing vessels.
"We found that chronic stress activates the sympathetic nervous system (SNS) — better known as the 'fight-or-flight' response — to profoundly impact lymphatic function and the spread of cancer cells. These findings demonstrate an instrumental role for stress and suggest that blocking the effects of stress to prevent cancer spread through lymphatic routes may provide a way to improve outcomes for patients with cancer," said Dr. Caroline Le, one of the study's lead researchers.
Once researchers found that stress induces the production of adrenaline, they went on to see whether blocking the adrenaline production through a commonly used blood pressure drug can prevent cancer metastasis.
The drug propanol was used on stressed mice with breast cancer. They found that the drug stopped their stress hormones from remodeling the lymph vessels inside the tumor, and reduced the risk of cancer spreading through the lymphatic system.
Reference: Caroline P. Le, Erica K. Sloan et al. Chronic stress in mice remodels lymph vasculature to promote tumor cell dissemination, Nature Communications 2016, doi:10.1038/ncomms10634.
Source: Medindia
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They found that high levels of stress triggers the production of adrenaline by the activation of sympathetic nervous system (SNS) that causes large amount of fluids to enter into the lymphatic system. The entry of fluids causes the lymphatic system to expand, resulting in high fluid inflow and outflow.
The researchers describe this mechanism as "lymphatic highway" which influences the cancer cells to spread through the body. Adrenaline not only increases the number of lymphatic vessels draining from the tumor but also increase the flow in existing vessels.
"We found that chronic stress activates the sympathetic nervous system (SNS) — better known as the 'fight-or-flight' response — to profoundly impact lymphatic function and the spread of cancer cells. These findings demonstrate an instrumental role for stress and suggest that blocking the effects of stress to prevent cancer spread through lymphatic routes may provide a way to improve outcomes for patients with cancer," said Dr. Caroline Le, one of the study's lead researchers.
Once researchers found that stress induces the production of adrenaline, they went on to see whether blocking the adrenaline production through a commonly used blood pressure drug can prevent cancer metastasis.
The drug propanol was used on stressed mice with breast cancer. They found that the drug stopped their stress hormones from remodeling the lymph vessels inside the tumor, and reduced the risk of cancer spreading through the lymphatic system.
Reference: Caroline P. Le, Erica K. Sloan et al. Chronic stress in mice remodels lymph vasculature to promote tumor cell dissemination, Nature Communications 2016, doi:10.1038/ncomms10634.
Source: Medindia
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