Chronic stress promotes tumor growth and angiogenesis in a mouse model of ovarian carcinoma

Thaker, Premal H.; Han, Liz Y.; Kamat, Aparna A.; Arevalo, Jesusa M.G.; Takahashi, Rie; Lü, Chunhua; Jennings, Nicholas B.; Armaiz-Pena, Guillermo N.; Bankson, James A.; Ravoori, Murali; Merritt, William M.; Lin, Yvonne G.; Mangala, Lingegowda S.; Kim, Tae Jin; Coleman, Robert L.; Landen, Charles N.; Yang, Li; Felix, Edward; Sanguino, Ángela; Newman, Robert A.; Lloyd, Mary; Gershenson, David M.; Kundra, Vikas; López-Berestein, Gabriel; Lutgendorf, Susan K.; Cole, Steven W.; Sood, Anil K.

doi:10.1038/nm1447

Cited by 1,107 publications

(1,283 citation statements)

References 22 publications

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“…Surveys of breast cancer survivors, and of those with no history of breast cancer, find that women commonly attribute the experience of stress as a contributory cause of this disease [2][3][4]. This view is supported by animal modelbased psychoneuroimmunological evidence concerning the effects of behavioural stress on tumorigenesis and the biological mechanisms involved [5][6][7]. In addition, psychological distress factors are known to be associated with established anthropometric, behavioural, and lifestyle factors that may contribute to tumour growth and development [5,[8][9][10].…”

Section: Introductionmentioning

confidence: 99%

No evidence that social stress is associated with breast cancer incidence

Surtees

Wainwright

Luben

et al. 2009

Breast Cancer Res Treat

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Women commonly attribute the experience of stress as a contributory cause of breast cancer. The purpose of this study is to investigate the associations between a history of social stress and breast cancer risk. A total of 11,467 women with no prior history of breast cancer, participants in the European Prospective Investigation into Cancer (EPIC)-Norfolk population-based prospective cohort study, completed a comprehensive assessment of lifetime social adversity exposure. Summary measures of social adversity were defined according to difficult circumstances in childhood, stressful life events and longer-term difficulties in adulthood, derived measures representing the subjective 'impact' of life events and associated 'stress adaptive capacity', and perceived stress over a 10-year period. Incident breast cancers were identified through linkage with cancer registry data. During 102,514 (median 9) personyears of follow-up, 313 incident breast cancers were identified. No associations were observed between any of the summary social adversity measures and subsequent breast cancer risk, with or without adjustment for age, menopausal status, parity, use of menopausal hormones, age at menarche, age at first birth, family history of breast cancer, physical activity, social class, body mass index, height, and alcohol intake. This study found no evidence that social stress exposure or individual differences in its experience are associated with the development of breast cancer. These findings may aid strategies designed to meet the psychosocial and emotional needs of breast cancer survivors and may be interpreted in a positive way in the context of commonly voiced beliefs that the experience of stress is a contributory cause of their disease.

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Section: Introductionmentioning

confidence: 99%

No evidence that social stress is associated with breast cancer incidence

Surtees

Wainwright

Luben

et al. 2009

Breast Cancer Res Treat

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“…potentiate the proliferation and migration of the cancer cells, inhibit the tumor cell apoptosis, increase the tumor cell invasiveness and metastatic activity, support the neoangiogenesis in the tumor tissue, or suppress the natural killer cell activity (Godbout and Glaser 2006;Sood et al 2006;Th aker et al 2006;Andersen et al 2007;Sephton et al 2009;Hassan et al 2013;Nagaraja et al 2013). Th ese eff ects are mediated especially by neurotransmitters released by sympathetic nerve endings, particularly by norepinephrine (Yang 2010).…”

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confidence: 99%

Sympathectomized tumor-bearing mice survive longer but develop bigger melanomas

Horváthová

Tillinger

Padová

et al. 2016

Endocrine Regulations

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Objectives.Previously we have shown that 20 days aft er the tumor cells injection smaller melanomas have been developed in chemically sympathectomized mice in comparison with animals having intact sympathetic nervous system. However, it is known that chemical sympathectomy reduces the sympathetic neurotransmission only temporarily. In the present study, we monitored the survival of the sympathectomized mice with melanoma with an attempt to fi nd out how long the suppressing eff ect of sympathectomy on the melanoma growth may endure.Methods. Th e chemical sympathectomy was performed by intraperitoneal injection of neurotoxin 6-hydroxydopamine in male C57BL/6J mice. Seven days later, the animals were injected subcutaneously with B16-F10 melanoma cells. Th en, melanoma development, survival of the tumorbearing mice and weight of the developed tumor mass were analyzed.Results. Sympathectomy delayed the development of the palpable tumors (18th day vs.14th day) and signifi cantly prolonged the survival of the tumor-bearing mice (median 34 days vs. 29 days). However, the weight of the developed melanoma was signifi cantly increased in the sympathectomized mice in comparison with the animals having intact sympathetic nervous system.Conclusions. Th e data of the present study showed that eff ect of the chemical sympathectomy, performed before the tumor growth induction, persisted even at the time when sympathetic nerves started to regenerate that resulted in a prolonged survival of the mice with melanoma. However, comparing to our previous study, in which we have shown a reduced tumor mass in earlier stages of the tumor growth, specifi cally 20 days aft er melanoma cells injection, now we indicate that in later stages of the melanoma progression, the tumor mass was signifi cantly increased in sympathectomized animals. Th ese contra-intuitive fi ndings may indicate that interventions aff ecting the sympathetic nervous system may exert complex eff ect on the tumor progression. Based on these data we may suggest that the potential therapeutic interventions aff ecting the sympathetic signaling in the tumor tissue and its microenvironment should attenuate the sympathetic neurotransmission not only temporarily but till the complete regression of the tumor tissue.

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“…Aside from causing suppression of CMI, CAs and PGs were shown to increase tumor cell invasion capacity, elevate VEGF secretion by malignant cells (2), and enhance tumor microvascular density (19,20). Accordingly, the blockade of CAs and PGs was indeed suggested to reduce cancer progression via multiple mechanisms (2,(20)(21)(22)(23).…”

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confidence: 99%

Improving Survival Rates in Two Models of Spontaneous Postoperative Metastasis in Mice by Combined Administration of a β-Adrenergic Antagonist and a Cyclooxygenase-2 Inhibitor

Glasner

Avraham

Rosenne

et al. 2010

The Journal of Immunology

217

177

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Clinical practice does not consider perioperative paracrine and neuroendocrine stress responses as risk factors for cancer recurrence, although recent animal studies provided supportive evidence. Suggested mechanisms include the effects of stress-hormones on tumor cells and on host physiology. In this study, in mice undergoing primary tumor excision, we tested the survival-enhancing potential of perioperative blockade of catecholamines and prostaglandins, and studied potential mediating mechanisms. C57BL/6J mice were inoculated intrafootpad with syngeneic B16F10.9-melanoma or Lewis lung carcinoma, and the paw was amputated when a developing tumor exceeded 100 μl. The clinically used β-adrenergic antagonist propranolol, and/or the cyclooxygenase-2 inhibitor etodolac, were administered once before amputation, and recurrence-free survival was monitored. In different studies, NK cytotoxicity, leukocytes' molecular functional markers, and vascular endothelial growth factor secretion by tumor cells were studied in the context of surgery and drug treatments. The findings indicated that the combination of propranolol and etodolac, but neither drug alone, significantly and markedly improved survival rates in both tumor models, and was as effective as established immunostimulatory agents (IL-12 and polyinosinic-polycytiylic acid). Surgery markedly reduced NK cytotoxicity and NK cell expression of Fas ligand and CD11a, reduced all circulating lymphocyte-subtype concentrations, and increased corticosterone levels. Propranolol and etodolac administration counteracted these perturbations. B16 and 3LL secreted vascular endothelial growth factor in vitro, but secretion was not affected by catecholamine agonists, prostaglandins, corticosterone, propranolol, or etodolac. Overall, propranolol and etodolac administration, which could be applied perioperatively in most cancer patients with minimal risk and low cost, has counteracted several immunologic and endocrinologic perturbations and improved recurrence-free survival rates in mice undergoing primary tumor excision.

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Chronic stress promotes tumor growth and angiogenesis in a mouse model of ovarian carcinoma

Cited by 1,107 publications

References 22 publications

No evidence that social stress is associated with breast cancer incidence

No evidence that social stress is associated with breast cancer incidence

Sympathectomized tumor-bearing mice survive longer but develop bigger melanomas

Improving Survival Rates in Two Models of Spontaneous Postoperative Metastasis in Mice by Combined Administration of a β-Adrenergic Antagonist and a Cyclooxygenase-2 Inhibitor

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