Abstract
Background: Mounting data suggest that exposure to chronic stress is associated with worse breast cancer outcomes. This study aimed to explore the impact of social environmental adversity (SEA, e.g., child abuse, crime, sexual, and physical violence), depressive symptomatology, and anxiety on immune cell infiltration into the breast tumor microenvironment. Methods: Participants (n = 33) completed a series of surveys assessing depression and anxiety symptoms, adverse childhood events (ACE), and trauma history. Tumor-associated macrophages (CD68+), B cells (CD19+), and T cells (CD3+) were identified by immunohistochemical analyses of formalin-fixed paraffin-embedded tumor samples and quantified. Spearman rank tests were used to explore the relationships between the variables studied. Results: Exposure to SEA was high (ACE = 72%, exposure to crime = 47%, and exposure to physical/sexual assault = 73%) among participants. Moreover, 30% reported a comorbid history of depression and ACE; 39% reported one or more traumatic events, and clinically significant depression symptomatology, while 21% reported trauma history and significant anxiety symptomatology. Increased tumor-infiltrating B cells were significantly correlated with exposure to crime, anxiety symptoms, and exposure to an ACE. The ACE plus anxiety group presented the highest infiltration of B cells, T cells, and macrophages. Conclusion: These findings support a role for SEA, anxiety symptoms, and depression as potential modulators of the immune tumor microenvironment in breast cancer.
Highlights
Breast cancer is the most common cancer diagnosed in women, with an estimated2.3 million new cases each year globally [1]
TheThe goalgoal of this was to examine whether breastbreast cancercancer patients exposed to so- to social environmental adversity (SEA, e.g., child abuse, crime, and sexual and cial environmental adversity (SEA, e.g., child abuse, crime, and sexual and physicalphysical vioviolence) and reporting symptoms of depression and anxiety correlated immune lence) and reporting symptoms of depression and anxiety correlated withwith immune cellscells infiltration in the breast tumor microenvironment
The theory’s neuroinflammatory-sensitization to adversity paradigm applied to the cancer experience may provide insights into known and novel biopsychosocial pathways (e.g., SEA, anxiety, depression, and adrenergic-mediated signaling) by which current and past exposure to chronic stress among breast cancer patients may lead to inflammatory phenotypes and cancer progression. These findings support a role for SEA, symptoms of anxiety, and depression as potential modulators of the immune tumor microenvironment in breast cancer
Summary
Breast cancer is the most common cancer diagnosed in women, with an estimated2.3 million new cases each year globally [1]. Mounting preclinical and clinical evidence supports a key role for the sustained activation of adrenergic-mediated signaling as a driver of tumor growth and progression, as well as decreased survival in various malignancies, including breast cancer [4,5,6,7,8]. Chronic sympathetic nervous system (SNS) activation induces inflammatory processes in the tumor microenvironment (TM) of several cancers [10] These (SNS and TM) are associated with the induction of growth-promoting signals primarily mediated by b-adrenergic receptors in tumor cells [11]. This study aimed to explore the impact of social environmental adversity (SEA, e.g., child abuse, crime, sexual, and physical violence), depressive symptomatology, and anxiety on immune cell infiltration into the breast tumor microenvironment. Conclusion: These findings support a role for SEA, anxiety symptoms, and depression as potential modulators of the immune tumor microenvironment in breast cancer
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