RGD Reference Report - Fatigue and proinflammatory cytokine activity in breast cancer survivors. - Rat Genome Database

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Fatigue and proinflammatory cytokine activity in breast cancer survivors.

Authors: Bower, JE  Ganz, PA  Aziz, N  Fahey, JL 
Citation: Bower JE, etal., Psychosom Med. 2002 Jul-Aug;64(4):604-11.
RGD ID: 8661748
Pubmed: PMID:12140350   (View Abstract at PubMed)

OBJECTIVE: Fatigue is a common problem among cancer patients and survivors, yet the mechanisms underlying the occurrence and persistence of this symptom are not known. Activation of the immune system may evoke feelings of fatigue, which are mediated by proinflammatory cytokines. We examined whether fatigued breast cancer survivors would show elevations in proinflammatory cytokines and markers of cytokine activity compared with nonfatigued survivors. Differences in lymphocyte subsets, cortisol, and behavioral symptoms associated with proinflammatory cytokines were also assessed. METHODS: Forty breast cancer survivors (20 fatigued, 20 nonfatigued) provided blood samples at visits scheduled to control for diurnal variability. Cytokines, soluble markers of cytokine activity, and cortisol were measured by immunoassay and lymphocyte subsets by flow cytometry. Participants also completed questionnaires measuring demographic, medical, and behavioral variables. RESULTS: Fatigued breast cancer survivors had significantly higher serum levels of several markers associated with proinflammatory cytokine activity than nonfatigued survivors, including interleukin-1 receptor antagonist (IL-1ra), soluble tumor necrosis factor receptor type II (sTNF-RII), and neopterin. They were also more likely to report behavioral problems that co-occur with fatigue in the context of immune activation. Fatigued survivors had significantly lower serum levels of cortisol than the nonfatigued group as well as differences in two lymphocyte populations. CONCLUSIONS: Fatigued breast cancer survivors showed elevations in serum markers associated with proinflammatory cytokine activity an average of 5 years after diagnosis. Results suggest mechanisms through which enduring immune activation may occur, including alterations in cortisol and in lymphocyte subsets.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
TNFRSF1BHumanFatigue  IEP protein:increased expression:serumRGD 
Tnfrsf1bRatFatigue  ISOTNFRSF1B (Homo sapiens)protein:increased expression:serumRGD 
Tnfrsf1bMouseFatigue  ISOTNFRSF1B (Homo sapiens)protein:increased expression:serumRGD 

Objects Annotated

Genes (Rattus norvegicus)
Tnfrsf1b  (TNF receptor superfamily member 1B)

Genes (Mus musculus)
Tnfrsf1b  (tumor necrosis factor receptor superfamily, member 1b)

Genes (Homo sapiens)
TNFRSF1B  (TNF receptor superfamily member 1B)


Additional Information