One Stage Posterior Minimal Laminectomy and Video-Assisted Thoracoscopic Surgery (VATS) for Removal of Thoracic Dumbbell Tumor.

OBJECTIVE: This study was conducted to assess the surgical results of one-stage posterior minimal laminectomy and video-assisted thoracoscopic surgery (VATS) for the treatment of thoracic dumbbell tumor and to describe its precise technique. In addition, we investigated the technique's usefulness and limitations. METHODS: Seven cases of thoracic dumbbell tumor (two men and five women, mean age, 43 years) were analyzed retrospectively. Pathological findings included schwannoma in four patients, neurofibroma in two patients, and hemangioma in one patient. The location of tumors varied from T2/3 to T12/L1. Dumbbell tumors were resected by one-stage operation using posterior laminectomy followed by VATS without instrumentation. Clinical data were reviewed. RESULTS: The mean follow-up period was 25 months (range, 3-58 months), and the operative time ranged from 255 to 385 min (mean, 331 min), with estimated blood loss ranging from 110 to 930 mL (mean, 348 mL). The tumor was completely resected without instrumentation and postoperative instability in all cases. Postoperative complications included atelectasis and facial anhydrosis in one case each. CONCLUSION: One-stage posterior minimal laminectomy and VATS may be a safe and less invasive technique for removal of thoracic dumbbell tumor without instability. This method has the advantage of early ambulation and rapid recovery because it reduces blood loss and postoperative pain.

Identification of a novel partner gene, KIAA1217, fused to RET: Functional characterization and inhibitor sensitivity of two isoforms in lung adenocarcinoma.

REarranged during Transfection (RET) fusion genes are detected in approximately 1% of lung adenocarcinomas and known primarily as oncogenic driver factors. Here, we found a novel RET fusion gene, KIAA1217-RET, and examined the functional differences of RET51 and RET9 protein, fused with KIAA1217 in cancer progression and drug response. KIAA1217-RET, resulting from the rearrangement of chromosome 10, was generated by the fusion of KIAA1217 exon 11 and RET exon 11 from a non-small cell lung cancer patient. Expression of this gene led to increased cell growth and invasive properties through activations of the PI3K/AKT and ERK signaling pathways and subsequently enabled oncogenic transformation of lung cells. We observed that cells expressing KIAA1217-RET9 fusion protein were more sensitive to vandetanib than those expressing KIAA1217-RET51 and both isoforms attenuated cellular growth via cell cycle arrest. These results demonstrated that KIAA1217-RET fusion represents a novel oncogenic driver gene, the products of which are sensitive to vandetanib treatment, and suggested that the KIAA1217-RET-fusion gene is a promising target for lung cancer treatment.