Reversal of neurochemical aberrations after tumor resection in rats

Chance, William T.; Cao, Lequn; Nelson, Jeffrey L.; Foley-Nelson, Terri; Fischer, Josef E.

doi:10.1016/s0002-9610(88)80269-1

Cited by 23 publications

(16 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is observed in a variety of species and with a variety of different viral and bacterial infections [53][54][55], in the presence of tumors [56], in response to endotoxin [57], and following administration of certain purified cytokines. IL-1 is particularly potent, and is effective when administered intracerebrally or by one of many other routes [53,54,57,58].…”

Section: Roles For Cytokines In Eliciting Sickness Behavior In Animalsmentioning

confidence: 99%

A Cytokine-Based Neuroimmunologic Mechanism of Cancer-Related Symptoms

Lee¹,

Dantzer

Langley

et al. 2004

Neuroimmunomodulation

264

184

View full text Add to dashboard Cite

While many of the multiple symptoms that cancer patients have are due to the disease, it is increasingly recognized that pain, fatigue, sleep disturbance, cognitive dysfunction and affective symptoms are treatment related, and may lead to treatment delays or premature treatment termination. This symptom burden, a subjective counterpart of tumor burden, causes significant distress. Progress in understanding the mechanisms that underlie these symptoms may lead to new therapies for symptom control. Recently, some of these symptoms have been related to the actions of certain cytokines that produce a constellation of symptoms and behavioral signs when given exogenously to both humans and animals. The cytokine-induced sickness behavior that occurs in animals after the administration of infectious or inflammatory agents or certain proinflammatory cytokines has much in common with the symptoms experienced by cancer patients. Accordingly, we propose that cancer-related symptom clusters share common cytokine-based neuroimmunologic mechanisms. In this review, we provide evidence from clinical and animal studies that correlate the altered cytokine profile with cancer-related symptoms. We also propose that the expression of coexisting symptoms is linked to the deregulated activity of nuclear factor-kappa B, the transcription factor responsible for the production of cytokines and mediators of the inflammatory responses due to cancer and/or cancer treatment. These concepts open exciting new avenues for translational research in the pathophysiology and treatment of cancer-related symptoms.

show abstract

Section: Roles For Cytokines In Eliciting Sickness Behavior In Animalsmentioning

confidence: 99%

A Cytokine-Based Neuroimmunologic Mechanism of Cancer-Related Symptoms

Lee¹,

Dantzer

Langley

et al. 2004

Neuroimmunomodulation

264

184

View full text Add to dashboard Cite

show abstract

“…Another area of tumor-induced alterations in metabolism is the increased rate of production of dopamine in the brain [26]. Among the sequelae of elevations in brain dopamine levels is the development of cachexia [27].…”

Section: Discussionmentioning

confidence: 99%

Effect of prostaglandin E in multiple experimental models: V. Effect on tumor/host interaction

Waymack¹,

1990

Journal of Surgical Oncology

View full text Add to dashboard Cite

Prostaglandin E (PGE) has long been incriminated as a cause of the immunosuppression seen in cancer patients and for the increased rates of tumor growth due to the impairment of the immunologic response to the tumor. We have investigated the effect of PGE on tumor-host interaction by utilizing a parenterally administered long-acting PGE derivative, 16,16-dimethyl-prostaglandin E (dPGE). Administration of dPGE was found to decrease the rate of tumor growth but at a cost of decreasing tumor-free body mass. The dPGE did not alter resting metabolic rates but did alter some parts of brain dopamine metabolism and significantly decreased the serum level of multiple amino acids. In conclusion, elevated PGE levels may significantly alter metabolism in tumor patients.

show abstract

“…These tubes were centrifuged (2,500 g, 4 • C) for 20 min, and the plasma was stored at -80 • C to await assay. The brains were removed rapidly from the skulls, with the hypothalamus being dissected free as described previously (23) and sectioned into halves prior to freezing in liquid nitrogen. Gastrocnemius, soleus, and extensor digitorum longus (EDL) muscles were also taken and frozen in liquid nitrogen prior to assay for protein and uncoupling protein messenger RNA (mRNA).…”

Section: Methodsmentioning

confidence: 99%

Continuous Intravenous Infusion of Ghrelin Does Not Stimulate Feeding in Tumor-Bearing Rats

Chance

Dayal

Friend

et al. 2007

Nutrition and Cancer

View full text Add to dashboard Cite

The development of anorexia continues to be a serious treatment issue for cancer patients. Because the orexigenic peptide, ghrelin, is active through systemic routes and activates hypothalamic neuropeptide systems known to be refractory in anorectic tumor-bearing (TB) rats, we investigated whether it would prevent the development of cancer anorexia when infused continuously intravenously. The 24-h food intake was increased in nontumor-bearing (NTB) rats at a dose of 288 microg/day ghrelin. However, no tested dose of ghrelin, up to 576 microg/day, elicited increased feeding in TB rats prior to or subsequent to the development of anorexia. In hypothalamus, ghrelin-infused TB rats exhibited significantly increased concentration of neuropeptide Y (NPY) as compared to saline-infused TB rats. Hypothalamic expression of NPY and agouti-related protein (AgRP) messenger RNA were elevated in ghrelin-infused TB rats as compared to NTB rats, but saline-infused TB rats also exhibited increased expression of AgRP. Proopiomelanocortin message was reduced in ghrelin-infused and saline-infused TB rats as compared to noninfused TB control rats. Although ghrelin infusion did not preserve muscle protein, a significant saving in body fat was observed in TB rats. Thus, the adiposity effects of ghrelin did not require an orexigenic response to the peptide. These results suggest that continuous ghrelin infusion may not be an effective treatment for cancer anorexia.

show abstract

Reversal of neurochemical aberrations after tumor resection in rats

Cited by 23 publications

References 13 publications

A Cytokine-Based Neuroimmunologic Mechanism of Cancer-Related Symptoms

A Cytokine-Based Neuroimmunologic Mechanism of Cancer-Related Symptoms

Effect of prostaglandin E in multiple experimental models: V. Effect on tumor/host interaction

Continuous Intravenous Infusion of Ghrelin Does Not Stimulate Feeding in Tumor-Bearing Rats

Contact Info

Product

Resources

About