Cancer patients frequently suffer concomitantly from loss of muscle mass, fatigue and depression. Understanding cancer-related fatigue (CRF) is critical because it negatively influences quality of life, functional independence, and survival. In the present study, we used a mouse model of tumor progression to discriminate between two main components of fatigue: loss of muscle mass/function and altered mood/motivation. Here we show that tumor progression over time was associated with increased fatigue, reduced body and muscle mass, and increased depressive-like behavior. Tumor induced fatigue, however, was independent of the functional capabilities of skeletal muscle. Moreover, fatigue, depressive-like behavior and increased cytokine expression in the brain were evident in tumor bearing mice within the first 2 weeks and preceded the loss of body and muscle mass. For example, within 2 weeks of tumor progression there was reduced voluntary wheel running activity and increased depressive-like behavior (e.g., resignation and anhedonia) that was not associated with general malaise or reduced muscle mass and contractile function. In addition, these changes in motivation and mood were paralleled by increased expression of IL-1β in the brain. Last, administration of minocycline, an anti-inflammatory agent and microglial inhibitor, ameliorated the tumor-induced increase in brain IL-1β expression, depressive-like behavior and fatigue. Taken together, these results indicate that inflammation and depressed mood are important early contributors to decreased physical activity and weakness associated with CRF.

A retrospective case review was carried out to report the outcomes in a contemporary case series of Ewing's sarcoma originating in the hand. We identified five patients treated since 1995. All five had wide surgical excision, one by ray amputation. All were treated with chemotherapy. Four patients also received radiation therapy, two to treat metastases and two as an adjunct to local excision. There were no local recurrences. Two patients developed metastases. Both died of their disease. Neither of these two patients had received local postoperative radiation therapy; one did not receive chemotherapy before definitive surgery. The other three patients were alive and free of disease at last follow-up, 4 to 12 years after initial presentation.

In this pilot study, hypertonic dextrose solution was used to induce fibrosis of the subsynovial connective tissue (SSCT) and create an animal model of potential use in the study of carpal tunnel syndrome (CTS). The SSCT of the carpal tunnel in 15 New Zealand white rabbits were injected with 0.05 ml of 10% dextrose solution in 1 paw and 0.05 ml of saline in the contralateral paw, to serve as a control. The animals were killed at 1, 2, 4, 8, or 12 weeks. While the saline side showed minimal changes at any time period, the hypertonic dextrose side showed progressive noninflammatory SSCT fibrosis, with vascular proliferation and thickening of collagen bundles. Demyelination of the median nerve developed at 12 weeks after the injection on the dextrose side. These findings are similar to the progression of pathology noted in humans with CTS.