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Tumor necrosis factor alpha (TNF-a) is one of the best-described cell death promoters. In murine L929 fibroblasts, dexamethasone inhibits TNF-a-induced cytotoxicity. Since phosphatidyl inositol 3 kinase (PI3K) and nuclear factor kappa B (NF-jB) proteins regulate several survival pathways, we evaluated their participation in dexamethasone protection against TNF-a cell death. We interfered with these pathways by overexpressing a negative dominant mutant of PI3K or a non-degradable mutant of inhibitor of NF-jB alpha (IjBa) (the cytoplasmic inhibitor of NF-jB) in L929 cells. The mutant IjB, but not the mutant PI3K, abrogated dexamethasone-mediated protection. The loss of dexamethasone protection was associated with a diminished accumulation in XIAP and c-IAP proteins.

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Upper thoracic tumors may develop spinal cord compression. By surgery at the time of diagnosis, a neurological deficit can be avoided. However, this particular localization requires a double approach to decompress the spinal cord and thoracic structures. The posterior extracavitary approach results in resection of the spinal canal, the foraminal component, and the extraspinal fragment, but is not routinely used by most neurosurgeons. A 56-year-old woman with a two-month history of axial thoracic pain and cough. The patient has a normal neurological examination. Thoracic computed tomography (CT) scan with contrast agent was performed, evincing a dumbbell-shaped tumor on the left T3-T4. Magnetic resonance imaging (MRI) confirms the diagnosis, showing a 4 cm diameter tumor that compresses the spinal cord without myelopathy. The surgery was performed posteriorly, with costotransversectomy, allowing complete resection under intraoperative neurophysiological monitoring. The patient developed no thoracic or neurological complications. One-stage posterior approach is possible and effective during the treatment of the upper thoracic dumbbell-shaped tumors, avoiding a change in surgical position, thoracic morbidity, and dependence on assisting surgeons.

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