Stress increases metastatic spread of a mammary tumor in rats: Evidence for mediation by the immune system

Ben‐Eliyahu, Shamgar; Yirmiya, Raz; Liebeskind, John C.; Taylor, Anna N.; Gale, Robert Peter

doi:10.1016/0889-1591(91)90016-4

Cited by 221 publications

(90 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Finally, relevant animal studies have come from the laboratory of Liebeskind and colleagues (Ben-Eliyahu, Yirmirya, Liebeskind, Taylor, & Gale, 1991) that suggest a link between paininduced immune suppression of NK cell activity and the development of syngenetic mammary tumors. In this model, tumor development and metastatic spread has been shown to be significantly controlled by NK cells.…”

Section: Biological Pathwaysmentioning

confidence: 99%

“…In addition to estrogen receptor status (an important prognostic indicator) predicting NK cell lysis, social support added significantly to the model in predicting higher NK cell activity. These data are somewhat inconsistent but are generally in line with data from healthy individuals with positive indicators of quality of life (e.g., social adjustment) predicting higher NK cell levels and negative-distress indicators (e.g., emotional distress) predicting lower NK cell levels.Finally, relevant animal studies have come from the laboratory of Liebeskind and colleagues (Ben-Eliyahu, Yirmirya, Liebeskind, Taylor, & Gale, 1991) that suggest a link between paininduced immune suppression of NK cell activity and the development of syngenetic mammary tumors. In this model, tumor development and metastatic spread has been shown to be significantly controlled by NK cells.…”

mentioning

confidence: 99%

See 1 more Smart Citation

A biobehavioral model of cancer stress and disease course.

Andersen¹,

Kiecolt‐Glaser²,

Glaser³

1994

American Psychologist

388

246

View full text Add to dashboard Cite

Approximately 1 million Americans are diagnosed with cancer each year and must cope with the disease and treatments. Many studies have documented the deteriorations in quality of life that occur. These data suggest that the adjustment process is burdensome and lengthy. There is ample evidence showing that adults experiencing other long-term stressors experience not only high rates of adjustment difficulties (e.g., syndromal depression) but important biologic effects, such as persistent downregulation of elements of the immune system, and adverse health outcomes, such as higher rates of respiratory tract infections. Thus, deteriorations in quality of life with cancer are underscored if they have implications for biological processes, such as the immune system, relating to disease progression and spread. Considering these and other data, a biobehavioral model of adjustment to the stresses of cancer is offered, and mechanisms by which psychological and behavioral responses may influence biological processes and, perhaps, health outcomes are proposed. Finally, strategies for testing the model via experiments testing psychological interventions are offered.Cancer is a major health problem, accounting for 23% of all deaths in the United States. Although death rates from heart diseases, stroke, and other conditions have been decreasing, deaths due to cancer have risen 20% in the past 30 years (American Cancer Society [ACS], 1993). This "big picture" holds for the major sites of disease, including lung, breast, and prostate cancer, for which death rates have shown large increases. The number-one killer, lung cancer, has shown huge increases in age-adjusted death rates in the past 30 years-an increase of 121% for men and 415% for women. The second most common site of cancer for men, prostate, has shown a 12% increase in the death rate. For women, breast cancer accounts for 32% of all new cases. During this decade alone, more than 1.5 million women (1 in 9) will be diagnosed and 30% of these women will die from the disease. Other sobering statistics indicate that since 1980 there has been a 24% increase in breast cancer incidence; despite major clinical studies (including trials of dramatic treatments, e.g., bone marrow transplantation), breast cancer mortality rates have been stable for the past 20 years. In sum, increasing numbers of individuals are being diagnosed, undergo difficult therapies, and somehow cope with 5-year relative survival rates of 53% for White Americans and 38% for Black Americans (ACS, 1993).Although there are notable exceptions (e.g., Bard & Sutherland, 1952;Fox, 1976), research programs conducted by psychologists on the behavioral and psychological aspects of cancer did not begin in earnest until the late 1970s. Yet considerable advances have been made in describing the difficulties cancer patients face and examining the processes of adjustment (see discussions in Andersen, 1989; Cancer, 1991, Vol. 67, No. 3 Supplement) NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manus...

show abstract

Section: Biological Pathwaysmentioning

confidence: 99%

mentioning

confidence: 99%

A biobehavioral model of cancer stress and disease course.

Andersen¹,

Kiecolt‐Glaser²,

Glaser³

1994

American Psychologist

388

246

View full text Add to dashboard Cite

show abstract

“…[10][11][12] Effects of biobehavioral factors on the immune system are thought to be mediated in part by the sympathetic nervous system, the HPA axis, and a variety of other hormones and peptides. 13,14 To date, the majority of neuroendocrinological research dealing with stress and accelerated tumor growth has focused on suppressed immune response to malignant tissue. 7 Recently, we and others have considered other biological pathways that may be affected by stress mediators.…”

Section: Introductionmentioning

confidence: 99%

The Neuroendocrine Impact of Chronic Stress on Cancer

Thaker¹,

Lutgendorf²,

Sood³

2007

Cell Cycle

129

View full text Add to dashboard Cite

Behavioral processes have long been suspected to influence many health processes including effects on cancer. However, mechanisms underlying these observations are not fully understood. Recent work has demonstrated that chronic behavioral stress results in higher levels of tissue catecholamines, greater tumor burden, and a more invasive pattern of ovarian cancer growth in an orthotopic mouse model. These effects are mediated primarily through the b 2 adrenergic receptor (ADRB2) activation of the tumor cell cyclic AMP (cAMP)-protein kinase A (PKA) signaling pathway. Additionally, tumors in stressed animals have increased vascularization and enhanced expression of vascular endothelial growth factor (VEGF) and matrix metalloproteinases (MMPs) -2 and -9. In this review, we highlight the importance of the neuroendocrine stress response in tumor biology and discuss mechanisms by which the b-adrenergic receptors on ovarian cancer cells enhance angiogenesis and tumor growth.

show abstract

“…These effects are thought to be mediated in part by the sympathetic nervous system, the HPA axis, and a variety of other hormones and peptides [8,[10][11][12][13]. In both animal and human studies, chronic stress has been shown to decrease cellular immune parameters, such as natural killer (NK) cell cytotoxicity and T-cell responses to mitogen stimulation [14][15][16].…”

Section: Introductionmentioning

confidence: 99%

Neuroendocrine influences on cancer biology

Thaker

Sood

2008

Seminars in Cancer Biology

View full text Add to dashboard Cite

Over the past 25 years, epidemiological and clinical studies have linked psychological factors such as stress, chronic depression, and lack of social support to the incidence and progression of cancer [1,2]. Although the mechanisms underlying these observations are not completely understood, recent molecular and animal studies have begun to identify specific signaling pathways that could explain the impact of neuroendocrine effects on tumor growth and metastasis. This review will highlight the importance of known clinical, molecular, and cellular processes with regard to the neuroendocrine stress effects on tumor biology and discuss possible behavioral and pharmacological interventions to ameliorate these effects and ultimately improve cancer outcomes.

show abstract

Stress increases metastatic spread of a mammary tumor in rats: Evidence for mediation by the immune system

Cited by 221 publications

References 27 publications

A biobehavioral model of cancer stress and disease course.

A biobehavioral model of cancer stress and disease course.

The Neuroendocrine Impact of Chronic Stress on Cancer

Neuroendocrine influences on cancer biology

Contact Info

Product

Resources

About