Marginating pulmonary-NK activity and resistance to experimental tumor metastasis: suppression by surgery and the prophylactic use of a β-adrenergic antagonist and a prostaglandin synthesis inhibitor

Melamed, Rivka; Rosenne, Ella; Shakhar, Keren; Schwartz, Yossi; Abudarham, Naphtali; Ben‐Eliyahu, Shamgar

doi:10.1016/j.bbi.2004.07.004

Cited by 193 publications

(213 citation statements)

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“…Within the NK cell population, a distinction was made between the small NK and the large NK subpopulations, because in previous studies we have repeatedly noticed molecular and functional differences between these populations (24,28). See Table I for detailed findings.…”

Section: Experiments 4: Comparing and Combining Poly(i:c) Immunostimulmentioning

confidence: 99%

“…The SKOV3 tumor line was provided by Dr. Anil K. Sood (University of Texas, Houston, TX). Cells were grown in cultures in 5% CO 2 , 100% humidity, 37˚C, in complete medium (CM) (24).…”

Section: Tumor Cell Linesmentioning

confidence: 99%

“…injection (22,24). The combined use of the blockers often was the only useful approach, suggesting a synergistic beneficial influence in the immediate postoperative context.…”

mentioning

confidence: 99%

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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

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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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Section: Experiments 4: Comparing and Combining Poly(i:c) Immunostimulmentioning

confidence: 99%

“…The SKOV3 tumor line was provided by Dr. Anil K. Sood (University of Texas, Houston, TX). Cells were grown in cultures in 5% CO 2 , 100% humidity, 37˚C, in complete medium (CM) (24).…”

Section: Tumor Cell Linesmentioning

confidence: 99%

See 1 more Smart Citation

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

Self Cite

218

177

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“…These agents are catecholamines, prostaglandins, and corticosteroids, which have been reported by Di Lorenzo et al [28], and Dokur et al [29]. These two groups have made a great contribution in this area, but Ben-Eliyahu et al [30,31] and Melamed [17] have done tremendous animal work in surgical immune suppression. By using the MADB-106 tumor model in rats they implicated sympathetic responses in supporting metastasis during stress and surgery.…”

mentioning

confidence: 98%

“…These are proinflammatory cytokines and many Type 2 immunosuppressive cytokines that interfere with (CMI) [16]. Melamed, Rosenne, Shakhar, et al [17] have shown the suppressive effect of surgery on NK cell activity in an animal model. They studied marinating pulmonary NK cell activity and resistance to experimental tumor metastasis and the suppression by surgery and the reversal of suppression by the prophylactic use of a β-adrenergic antagonist and a prostaglandin synthesis inhibitor.…”

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confidence: 99%

Cancer Immunothearapy More than Vaccines “Psychoneuro-Immunooncology: Cancer, the Host, and the Surgeon”

Elliott¹

2011

JCT

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Perioperative biobehavioral interventions to prevent cancer recurrence through combined inhibition of β‐adrenergic and cyclooxygenase 2 signaling

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Hanalis-Miller

Haldar

et al. 2018

Cancer

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Evidence suggests that excess perioperative activation of the sympathetic nervous system and the consequent release of catecholamines (ie, epinephrine and norepinephrine) in the context of cancer surgery and inflammation may significantly facilitate prometastatic processes. This review first presents biomedical processes that make the perioperative timeframe pivotal in determining long-term cancer outcomes nonproportionally to its short duration (days to weeks). Then, it analyzes the various mechanisms via which the excess release of catecholamines can facilitate the progression of cancer metastases in this context by directly affecting the malignant tissues and by regulating, via indirect pathways, immunological and other mechanisms that affect metastatic progression in the tumor microenvironment and systemically. In addition, this review addresses the need to supplement β-adrenoreceptor blockade with cyclooxygenase 2 inhibition, especially during surgery and shortly thereafter, because similar mechanisms are simultaneously activated by surgery-induced inflammatory responses. Importantly, this review presents translational and clinical evidence showing that perioperative β-adrenoreceptor blockade and cyclooxygenase 2 inhibition can reduce the prometastatic process and cancer recurrence, and the clinical feasibility and safety of this approach are demonstrated as well. Lastly, alternative psychophysiological approaches to the use of β-adrenergic blockers are presented because a substantial portion of patients have medical contraindications to this pharmacological treatment. The adaptation of existing psychophysiological interventions to the perioperative period and principles for constructing new approaches are discussed and exemplified. Overall, pharmacobehavioral interventions, separately or in combination, could transform the perioperative timeframe from being a prominent facilitator of metastatic progression to an opportunity for arresting or eliminating residual disease, potentially improving long-term survival rates in cancer patients. Cancer 2019;125:45-56.

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Marginating pulmonary-NK activity and resistance to experimental tumor metastasis: suppression by surgery and the prophylactic use of a β-adrenergic antagonist and a prostaglandin synthesis inhibitor

Cited by 193 publications

References 50 publications

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

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

Cancer Immunothearapy More than Vaccines “Psychoneuro-Immunooncology: Cancer, the Host, and the Surgeon”

Perioperative biobehavioral interventions to prevent cancer recurrence through combined inhibition of β‐adrenergic and cyclooxygenase 2 signaling

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