Exogenous APN protects normal tissues from radiation-induced oxidative damage and fibrosis in mice and prostate cancer patients with higher levels of APN have less radiation-induced toxicities.

Radiation causes damage to normal tissues that leads to increased oxidative stress, inflammation, and fibrosis, highlighting the need for the selective radioprotection of healthy tissues without hindering radiotherapy effectiveness in cancer. This study shows that adiponectin, an adipokine secreted by adipocytes, protects normal tissues from radiation damage invitro and invivo. Specifically, adiponectin (APN) reduces chronic oxidative stress and fibrosis in irradiated mice. Importantly, APN also conferred no protection from radiation to prostate cancer cells. Adipose tissue is the primary source of circulating endogenous adiponectin. However, this study shows that adipose tissue is sensitive to radiation exposure exhibiting morphological changes and persistent oxidative damage. In addition, radiation results in a significant and chronic reduction in blood APN levels from adipose tissue in mice and human prostate cancer patients exposed to pelvic irradiation. APN levels negatively correlated with bowel toxicity and overall toxicities associated with radiotherapy in prostate cancer patients. Thus, protecting, or modulating APN signaling may improve outcomes for prostate cancer patients undergoing radiotherapy.

Development of the PROMIS-based Research Assessment and Clinical Tool-Fatigue (ReACT-F).

PURPOSE: Evidence has shown that cancer-related fatigue (CRF) may be a treatment-limiting symptom and often impairs health-related quality of life. Accurate assessment of the multidimensional nature of CRF could help drive interventions to mitigate this debilitating symptom. Currently, there are no clinical tools to effectively and efficiently assess the multidimensionality of CRF. The purpose of this paper is to introduce a CRF-specific short form that can assess the multidimensional nature of CRF for use in the clinical setting. METHODS: The CRF-specific short form was developed using the 95-item PROMIS® fatigue bank. Bi-factor analysis was used to evaluate dimensionality of the alternative model using fatigue for the general factor and physical, cognitive, affective, global, and motivational for the local factors. After unidimensionality was confirmed (loading factor > 0.3), one item from each local factor was selected using discrimination power for inclusion in the CRF-specific short form. RESULTS: The Research Assessment and Clinical Tool-Fatigue (ReACT-F) was created from the 95-item PROMIS fatigue bank using established item parameters. The ReACT-F assesses five common dimensions of CRF as well as perceived burden of the fatigue dimensions. CONCLUSIONS: The ReACT-F is a CRF-specific self-report short form that addresses the need for a brief, clinically useful tool to quickly assess the multidimensional nature of CRF. We anticipate that the ReACT-F can be completed in the clinical setting in approximately 3 minutes, providing clinicians with meaningful data to drive personalized interventions. Further validation of the ReACT-F is highly encouraged.