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Roswell Park Researchers Identify Key Link Between Stress and Cancer

AHA Publisher — Mon, 08 Nov 2021 08:00:50 +0000

Roswell Park Comprehensive Cancer Center via Newswise – BUFFALO, N.Y. — Stress can have a significant negative effect on health, but our understanding of how stress impacts the development and progression of cancer is just beginning. A team from Roswell Park Comprehensive Cancer Center has identified an important mechanism by which chronic stress weakens immunity and promotes tumor growth. Their findings, just published in Cell Reports, point to the beta-adrenergic receptor (β-AR) as a driver of immune suppression and cancer growth in response to stress, opening the possibility of targeting this receptor in cancer therapy and prevention. Using a preclinical model of triple-negative breast cancer, a research team led by Hemn Mohammadpour, PhD, DVM, a postdoctoral research affiliate in the lab of Elizabeth Repasky, PhD, and Dr. Repasky, who is Co-Leader of the Cell Stress and Biophysical Therapies Program and the Dr. William Huebsch Professor in Immunology at Roswell Park, found that as tumors grow, they become more sensitive to stress signals coming from the nervous system. Specifically, the researchers discovered that a population of immune cells known as myeloid derived suppressor cells (MDSCs) show an increase in the expression of β-AR, a molecule that controls the function of key immune cells. The findings will help researchers better understand why prolonged exposure to stress often makes our immune system less effective, and build on Roswell Park’s pioneering research into the relationship between stress and cancer. “This increase in β-AR expression on myeloid-derived suppressor cells allows these cells to be stimulated by the stress hormone norepinephrine, which fosters an immunosuppressed environment that promotes tumor growth by increasing MDSCs’ ability to generate and process energy and suppress anti-tumor immune response,” says Dr. Mohammadpour, the paper’s first author. “This study provides some very important clues that help explain the specific mechanisms by which prolonged stress stimulates tumor growth and decreases lifespan.” While there has been a longstanding recognition that long periods of stress, or chronic activation of nerves, are harmful to overall health, details about how this occurs are unclear, especially in the setting of cancer. A better understanding of the specific ways in which stress influences cancer, particularly in terms of lowering immunity against tumor cells, could be used to design new drugs or therapies that can help to minimize negative effects of chronic stress and boost cancer immunotherapy. Based on these findings, Dr. Repasky’s team is planning new clinical and laboratory studies to identify therapies — including existing therapies already approved for other applications — that can block these harmful stress signals and stop the negative cycle of cancer growth and metastasis. “This is especially important for cancer patients, who frequently endure greatly increased levels of stress after their diagnosis, including anxiety, depression and worry about factors like finances and family interactions,” adds Dr. Mohammadpour. Several clinical trials are planned or underway to investigate which interventions are most effective at mitigating the effects of stress in patients with cancer. Roswell Park is currently studying the effects of combining the β-AR blocker propranolol, which is traditionally used to treat migraine headache and various heart problems, with immunotherapy. The study, “β2-adrenergic receptor signaling regulates metabolic pathways critical to myeloid-derived suppressor cell function within the TME,” was supported by the National Institutes of Health and National Cancer Institute (grants R01CA205246, R01CA099326, R01CA172105, F32CA239356, K99 HL155792, T32CA085183 and F30CA265127 and P30CA016056, Roswell Park’s core grant from the NCI) and by the Roswell Park Alliance Foundation. Co-authors include Philip McCarthy, MD, Professor of Oncology and Internal Medicine and Director of Roswell Park’s Transplant & Cellular Therapy Center; Scott Abrams, PhD, Co-Leader of Roswell Park’s Tumor Immunology and Immunotherapy Program; and Cameron MacDonald, a predoctoral trainee in immunology. To read the original article click here.

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How Does Chronic Stress Induce Bone Loss?

AHA Publisher — Mon, 14 Sep 2020 07:00:03 +0000

Chinese Academy of Sciences Headquarters via EurekAlert – Clinical studies have found that bone mineral density in patients with anxiety or depression is lower than in ordinary people. The brain, commander of the body, receives and processes external signals, and then sends instructions to peripheral bones. But how does anxiety induce a decline in bone mineral density? Researchers from the Shenzhen Institutes of Advanced Technology (SIAT) of the Chinese Academy of Sciences and their collaborators now have an answer. They found that a central neural circuit from the forebrain to the hypothalamus mediates chronic stress-induced bone loss via the peripheral sympathetic nervous system. Their study was published in the Journal of Clinical Investigation on September 10. The researchers found that isolation can significantly increase anxiety levels, thus inducing bone loss in human subjects. Biochemical analysis showed that prolonged isolation increases the concentration of norepinephrine and decreases osteogenic markers in serum. These changes were consistent with the observation of elevated anxiety and reduced bone formation in subjects. In order to identify the neural mechanism underlying chronic stress-induced bone loss, the research team used a mouse model where mice were subjected to unpredictable chronic mild stress. They found that after four to eight weeks of chronic stress, the mice displayed significant anxiety behaviors. The bone mineral density of the mice in the stress group was significantly lower than in the control group. These results confirmed the correlation between stress-induced anxiety and bone loss in experimental animals, and provided a good animal model for follow-up neural mechanism analysis. Through extensive experiments, researchers identified a population of inhibitory neurons expressing somatostatin in the brain nucleus that are known as the bed nucleus of the stria terminalis (BNST) in the forebrain. These neurons were activated when animals showed anxiety behaviors and transmitted “anxiety” information to the neurons in the ventromedial hypothalamus (VMH). “Activating the BNST-VMH neural circuit can simultaneously induce anxiety-like behaviors and generate bone loss in the mice, whereas inhibition of this circuit can prevent stress-induced anxiety and bone loss at the same time,” said Prof. YANG Fan from SIAT, the co-first and co-corresponding author of the study. Furthermore, the researchers discovered that glutamatergic neurons in nucleus tractus solitaries (NTS) and the sympathetic system were employed to regulate stress-induced bone loss. “This study provides a new perspective for the systematic study of the regulatory mechanism of brain homeostasis on metabolism and endocrine function of the body in special environments,” said Prof. WANG Liping, Director of the Brain Cognition and Brain Disease Institute of SIAT. To read the original article click here.

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Solving a Biological Puzzle: How Stress Causes Gray Hair

AHA Publisher — Wed, 29 Jan 2020 08:00:19 +0000

Harvard University via Science Daily – Scientists have found evidence to support long-standing anecdotes that stress causes hair graying. Researchers found that in mice, the type of nerve involved in the fight-or-flight response causes permanent damage to the pigment-regenerating stem cells in the hair follicle. The findings advance knowledge of how stress impacts the body and are a first step toward blocking its negative effects. To read the original article click here.

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