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Background: , which is highly up-regulated in oral cancer cells, has been reported to be aberrantly expressed in several cancers; however, the significance of miR-196 in oral cancer has not yet been addressed.

The pelvic girdle, thigh, and calf muscles of 29 patients with Duchenne muscular dystrophy (DMD) were evaluated with magnetic resonance (MR) imaging. The muscles that were most resistant to disease were the gracilis, followed by the sartorius, semitendinous, and semimembranous. Sixteen patients had asymmetric involvement in part of the muscle bundles of thigh. An MR grading system was developed to assess the number of preserved pelvic and thigh muscles, the severity of fatty infiltration of the calf, and the increase of subcutaneous fat. Statistically significant correlations were obtained between MR grade and clinical functional grade (P < .01), MR grade and disease duration (P < .01), and MR grade and patient age (P < .01). An inverse correlation was observed between the creatine kinase values and the MR grade (P < .05). The MR grading system helped identify disease severity in patients with low clinical functional grades. Twenty-four follow-up studies were performed in 22 patients. In 13 of the 24 cases, the MR grade progressed while the clinical functional grade remained unchanged. Both the MR and clinical functional grades progressed in six cases. The results suggest that MR imaging may be useful in prebiopsy mapping and may help accurately monitor the progression of DMD.

Radiotherapy is an integral part for the treatment of head and neck cancer (HNC), while radioresistance is a major cause leads to treatment failure. GDF15, a member of the TGF-β superfamily, is hypothesized to participate in various types of homeostasis. However, the potential role of this molecule in regulation of radiosensitivity remains unclear. In this study, we demonstrated that GDF15 contributed to radioresistance of HNC, as determined by both gain- and lost-of-functional experiments. These results were achieved by the induction of mitochondrial membrane potential and suppression of intracellular reactive oxygen species (ROS). We further showed that GDF15 facilitated the conversion of cancer stemness, as assessed by the promotion of CD44+ and ALDH1+ cell populations and spheroid cell formation. At molecular level, GDF15 conferred to these cellular functions was through phosphorylated SMAD1 proteins to elite downstream signaling molecules. These cellular results were further confirmed in a tumor xenograft mouse study. Taken together, our results demonstrated that GDF15 contributed to radioresistance and cancer stemness by regulating cellular ROS levels via a SMAD-associated signaling pathway. GDF15 may serve as a prediction marker of radioresistance and a therapeutic target for the development of radio-sensitizing agents for the treatment of refractory HNC.