The Central Response to Ovarian Carcinoma Simulates the Response to Sepsis

Carson, Linda F.; Roy, Sabita; Cain, Kelly; Charboneau, Richard; DeTurris, Stanley; Ramakrishin, S; Barke, Roderick A.

doi:10.1006/jsre.1997.5183

Cited by 8 publications

(5 citation statements)

References 19 publications

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“…The upregulation of IL-1b mRNA in the brain has been reported in tumor models using prostate adenocarcinoma [11], ovarian carcinoma [33], and mice bearing Ehrlich's ascites tumor cells [29]. Central tumor models involving the infusion of C6 glioma cells [34] and human carcinoma and glioma cells [35] into the central nervous system (CNS) of rodents also demonstrated the induction of IL-1b mRNA, supporting an increase in IL-1b levels in the brain during tumor growth.…”

Section: Discussionmentioning

confidence: 67%

Interleukin-1?? system in anorectic catabolic tumor-bearing rats

Turrin

Ilyin

Gayle

et al. 2004

Current Opinion in Clinical Nutrition and Metabolic Care

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Section: Discussionmentioning

confidence: 67%

Interleukin-1?? system in anorectic catabolic tumor-bearing rats

Turrin

Ilyin

Gayle

et al. 2004

Current Opinion in Clinical Nutrition and Metabolic Care

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“…The null-finding exceptions are rare (Carson et al, 1998; Wang et al, 2001). Mounting evidence indicates that this central cytokine production is tumor-initiated rather than host-derived (Baltgalvis et al, 2010; Cahlin et al, 2000; Kawamura et al, 1999; Rebeca et al, 2008).…”

Section: Rodent Models Of Cancermentioning

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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“…Indeed, our previous study showed that TNF-␣ injection into the intracerebroventricular space caused an increase in plasma corticosterone and catecholamine levels, leading to an enhancement of proteolysis and glucose production in rats [9]. Furthermore, cytokine mRNA levels in the brain are elevated in tumorbearing animals [10,11] and septic rats [12].…”

Section: Introductionmentioning

confidence: 98%