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Association of Mitochondrial Dysfunction with Cancer-Related Fatigue Intensification

Friday, September 18, 2015 — Poster Session IV

12:00 p.m. – 1:30 p.m.
FAES Terrace
NINR
BEHAV-9

Authors

  • KA Filler
  • R Feng
  • LN Saligan

Abstract

Background: The etiology of cancer-related fatigue (CRF) intensification during radiation therapy (RT) remains unknown, making it a challenging and a difficult symptom to manage and treat. We hypothesize that CRF intensification during RT is a result of mitochondrial dysfunction. Methods: Men with non-metastatic prostate cancer (NM-PC) receiving external beam RT (EBRT) were enrolled and fatigue was measured by the Functional Assessment of Cancer Therapy– Fatigue subscale (FACT-F). Participants were categorized into high fatigue intensification (HF) or low fatigue intensification (LF) groups, based on change in FACT-F scores during EBRT. Peripheral blood was obtained to measure mitochondrial-related enzymes and genes using ELISA and PCR. Results: Preliminary findings in men with NM-PC have shown increases in mitochondrial enzymes, decreases in SOD2, and lower hemoglobin in the HF group with opposite trends observed in the LF group during EBRT. Exploration of the gene expression is ongoing. Discussion: Concentrations of mitochondrial complex II enzymes significantly correlated with fatigue scores in all subjects at each time point, as well as in the HF group at baseline. Hemoglobin levels were significantly different between the HF and LF groups at each time point, suggesting that oxygenation status and a hypoxic cellular environment may contribute to the fatigue experience during EBRT, consistent with prior report. Conclusion: Understanding the etiology of CRF has significant clinical implications for personalizing cancer therapy and prospectively attenuating toxicity risk. Furthermore, this type of information provides patients and their families with more knowledge upon which to make optimal treatment decisions.

Category: Social and Behavioral Sciences