Abstract
The mechanisms behind fatigue intensification during cancer therapy remain elusive. The interferon alpha-inducible protein 27 (IFI27) was the most up-regulated gene based on our previous microarray data in fatigued men with non-metastatic prostate cancer receiving localized external beam radiation therapy (EBRT). The purpose of this study was to confirm the IFI27 up-regulation and determine its association with fatigue intensification during EBRT. Peripheral blood samples and fatigue scores were collected at three time points—prior to EBRT, at midpoint, and at completion of EBRT. Confirmatory quantitative real time polymerase chain reaction (qPCR) and enzyme-linked immunosorbent assay (ELISA) were utilized to verify the microarray results. Subjects were a total of 40 Caucasian men with prostate cancer; 20 scheduled for EBRT (65.6 ± 7.5 years old), and 20 on active surveillance as controls (62.8 ± 6.1 years old). Significant IFI27 expression overtime during EBRT was confirmed by qPCR (p < 0.5), which correlated with fatigue scores during EBRT (R = −0.90, p = 0.006). Alterations in mechanisms associated with immune response and mitochondrial function that explain the up-regulation of IFI27 may provide an understanding of the pathways related to the intensification of fatigue during localized radiation therapy.
Highlights
Improvement in prostate cancer treatment, especially with the use of modulated radiation therapy has increased cure and survival rates [1]
We recently reported profiles of gene expression changes over time during radiation therapy in men treated with non-metastatic prostate cancer, suggesting that mitochondrial dysfunction [19] and neuroinflammatory pathways [20] may play a role in fatigue development and intensification during external beam radiation therapy (EBRT)
The total sample of 40 men with non-metastatic prostate cancer consisted of 20 men who received
Summary
Improvement in prostate cancer treatment, especially with the use of modulated radiation therapy has increased cure and survival rates [1]. Fatigue severity in most men with non-metastatic prostate cancer is known to increase significantly during the course of radiation therapy (RT) peaking at midpoint and declining after completion of the RT [4]. A recent review revealed the lack of longitudinal studies that can explain physiologic mechanisms behind intensification of fatigue during cancer therapy [5]. Studies reported associations between immune and inflammatory markers with the worsening intensity of cancer-related fatigue (CRF) during therapy [6,7,8,9,10], no compelling data between a specific biomarker and CRF has been established, contributing to its inadequate clinical management
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