Interleukin-6 levels and HPA axis activation in breast cancer patients with major depressive disorder

Soygür, Haldun; Palaoǧlu, Özden; Akarsu, Eyüp S.; Cankurtaran, Eylem Şahin; Özalp, Elvan; Turhan, Levent; Ayhan, I.H.

doi:10.1016/j.pnpbp.2007.05.001

Cited by 73 publications

(69 citation statements)

References 30 publications

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“…Evidence from studies on experimental animals and human and clinical trials have suggested that depression may influence BC development through several mechanisms, such as interfering with the DNA repair mechanism and triggering the abnormal activity of the hypothalamicpituitary-adrenal axis (21). Likewise, chest X-ray exposure after puberty was also found to be a significant risk for BC in North Cyprus women.…”

Section: Discussionmentioning

confidence: 99%

Risk factor assessment for breast cancer in North Cyprus: a comprehensive case-control study of Turkish Cypriot women

2018

Turk J Med Sci

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Section: Discussionmentioning

confidence: 99%

Risk factor assessment for breast cancer in North Cyprus: a comprehensive case-control study of Turkish Cypriot women

2018

Turk J Med Sci

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“…In ovarian cancer patients with invasive disease, elevated IL-6 in plasma and ascites is associated with greater somatic, but not affective, symptoms of depression prior to diagnosis (Lutgendorf et al, 2008). In breast cancer patients prior to the receipt of treatment, a diagnosis of depression by structured interview (Structured Clinical Interview for DSM-IV, SCID) is associated with both elevated plasma IL-6 and abnormal dexamethasone suppression tests compared to non-depressed patients (Soygur et al, 2007). Similarly, levels of soluble IL-6 receptor (sIL-6r) and CRP are positively associated with fatigue and affective symptoms of depression in breast cancer patients prior to treatment (Courtier et al, 2013; Pertl et al, 2013).…”

Section: Cancer Patients Prior To Treatmentmentioning

confidence: 99%

Pre-treatment effects of peripheral tumors on brain and behavior: Neuroinflammatory mechanisms in humans and rodents

Schrepf¹,

Lutgendorf²,

Pyter³

2015

Brain, Behavior, and Immunity

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Cancer patients suffer high levels of affective and cognitive disturbances, which have been attributed to diagnosis-related distress, impairment of quality of life, and side effects of primary treatment. An inflammatory microenvironment is also a feature of the vast majority of solid tumors. However, the ability of tumor-associated biological processes to affect the central nervous system (CNS) has only recently been explored in the context of symptoms of depression and cognitive disturbances. In this review, we summarize the burgeoning evidence from rodent cancer models that solid tumors alter neurobiological pathways and subsequent behavioral processes with relevance to affective and cognitive disturbances reported in human cancer populations. We consider, in parallel, the evidence from human clinical cancer research demonstrating that affective and cognitive disturbances are common in some malignancies prior to diagnosis and treatment. We further consider the underlying neurobiological pathways, including altered neuroinflammation, tryptophan metabolism, prostaglandin synthesis and associated neuroanatomical changes, that are most strongly implicated in the rodent literature and supported by analogous evidence from human cancer populations. We focus on the implications of these findings for behavioral researchers and clinicians, with particular emphasis on methodological issues and areas of future research.

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“…The glutamate hypothesis of depression was proposed by Skolnick et al [48] and modified later [47,49]. Based on the antidepressantlike activity of NMDA/glutamate receptor antagonists a link between hyperactivity of the glutamate system and depression was indicated [19,48,49,53,65]. Additionally, glutamate receptor antagonists or its modulators showed antidepressant properties in treatment refractory depression [1,9,13,14,27,28,41,44,71,72].…”

Section: Zinc Deficiency Alters Responsiveness To Antidepressantsmentioning

confidence: 99%

“…Cytokines have been shown to stimulate the expression and release of the corticotropin-releasing hormone (CRH) and adrenocorticotropic hormone (ACTH), as well as cortisol; all of which have been found to be elevated in patients with depression. IL-6 might change the negative feedback, resulting in the down-regulation of corticosteroid receptors [53]. It was found that patients suffering from depression exhibit increased inflammatory cytokines, such as IL-6, which positively correlated with plasma cortisol [25].…”

Section: Zinc Deficiency Alters Responsiveness To Antidepressantsmentioning

confidence: 99%

Zinc deficiency alters responsiveness to antidepressant drugs in mice

Młyniec

Budziszewska

Reczyński

et al. 2013

Pharmacological Reports

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Abstract:Background: There is some evidence coming from preclinical and clinical studies suggesting a relationship between dietary zinc intake and depressive symptoms. The aim of the study was to determine whether zinc deficiency alters the response to antidepressants with a different mechanism of action. We examine also whether these changes are related to activity of the hypothalamic-pituitaryadrenal HPA axis. Methods: Male CD-1 mice were assigned to groups according to diet and antidepressant administration. To evaluate animal behavior, the immobility time in the forced swim test (FST) and locomotor activity were measured. To determine serum zinc levels the flame atomic absorption spectroscopy (FAAS) was used. The serum corticosterone was determined by radioimmunoassay (RIA). Results: Antidepressants administered to zinc-deprived mice induced an altered response in the FST when compared to animals fed with an adequate diet. There were no changes in locomotor activity. Animals subjected to a zinc-deficient diet showed a significant reduction in serum zinc levels, which was normalized by antidepressant treatment. An increase in serum corticosterone concentrations in mice fed with a zinc-deficient diet and treated with antidepressants was observed, so it can be concluded that reduced levels of zinc contribute hyperactivation of the HPA axis. Conclusion:The results of this study suggest that a diet with a reduced zinc level alters antidepressant action, which is associated with a reduction in the serum zinc level and rise in the corticosterone level. The results of this study may indicate the involvement of zinc deficiency in the pathogenesis of depression.

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Interleukin-6 levels and HPA axis activation in breast cancer patients with major depressive disorder

Cited by 73 publications

References 30 publications

Risk factor assessment for breast cancer in North Cyprus: a comprehensive case-control study of Turkish Cypriot women

Risk factor assessment for breast cancer in North Cyprus: a comprehensive case-control study of Turkish Cypriot women

Pre-treatment effects of peripheral tumors on brain and behavior: Neuroinflammatory mechanisms in humans and rodents

Zinc deficiency alters responsiveness to antidepressant drugs in mice

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