Conclusion: This is the first report on human sentinel node (SN) detection by interstitial magnetic resonance (MR) lymphography with superparamagnetic iron oxide (SPIO) in tongue cancer patients who also underwent lymphoscintigraphy. Our results indicate that further studies are warranted, as this novel method may replace current scintigraphic techniques. Objectives: To examine the feasibility of interstitial MR lymphography using SPIO for SN detection in the head and neck region. Methods: MR images were acquired sequentially at 10 min, 30 min, and 24 h after submucosally injecting 0.1 ml SPIO (ferucarbotran) around the tumor in three patients with tongue cancer without cervical lymph node metastasis (clinical T2N0M0). Results: The SNs were clearly visualized in the 10 min interstitial MR lymphography images and were completely concordant with those visualized by ^99mTc-radiocolloid lymphoscintigraphy and a gamma probe in all cases. Iron incorporation into the SNs was confirmed by pathological examination.

Acquired tracheal stenosis remains a challenging problem for otolaryngologists. The objective of this study was to determine whether the Sendai virus (SeV)-mediated c-myc suppressor, a far upstream element (FUSE)-binding protein (FBP)-interacting repressor (FIR), modulates wound healing of the airway mucosa, and whether it prevents tracheal stenosis in an animal model of induced mucosal injury. A fusion gene-deleted, non-transmissible SeV vector encoding FIR (FIR-SeV/ΔF) was prepared. Rats with scraped airway mucosae were administered FIR-SeV/ΔF through the tracheostoma. The pathological changes in the airway mucosa and in the tracheal lumen were assessed five days after scraping. Untreated animals showed hyperplasia of the airway epithelium and a thickened submucosal layer with extensive fibrosis, angiogenesis, and collagen deposition causing lumen stenosis. By contrast, the administration of FIR-SeV/ΔF decreased the degree of tracheal stenosis (P < 0.05) and improved the survival rate (P < 0.05). Immunohistochemical staining showed that c-Myc expression was downregulated in the tracheal basal cells of the FIR-SeV/ΔF-treated animals, suggesting that c-myc was suppressed by FIR-SeV/ΔF in the regenerating airway epithelium of the injured tracheal mucosa. The airway-targeted gene therapy of the c-myc suppressor FIR, using a recombinant SeV vector, prevented tracheal stenosis in a rat model of airway mucosal injury.