Background: Conventional microsurgical approaches are limited to exposing the lateral and bilateral regions because of surgical trauma. Total removal of clival chordoma and chondrosarcoma is very difficult. This study was undertaken to determine the potential role of an endoscopic endonasal approach in improved management of clival chordoma and chondrosarcoma. Methods: Seven patients with chordoma and 2 patients with chondrosarcoma treated by endoscopic endonasal surgery between November 2002 and February 2006 were studied prospectively. The mean age was 35 years. The follow-up periods ranged from 3 to 39 months. Results: Total removal was achieved in 6 cases of chordoma and 1 case of chondrosarcoma, with subtotal removal in 1 case of chordoma and of chondrosarcoma. At the last follow-up, 7 patients had no evidence of disease and 1 was alive with disease. The chordomas had recurred in 1 patient after 5 months with subtotal removal. Conclusion: The use of nasoendoscopy to perform clival chordoma and chondrosarcoma surgery is not limited to merely the minimally invasive aspects. It provides better visualization of the deeper anatomical structures in the skull base and affords a means to ‘look around corners’. This approach promises a simple and rapid access to the clivus. It is both a safe and efficient procedure.

Oxymatrine may inhibit tumor cell proliferation, induce cell cycle arrest, promote apoptosis, induce tumor cell differentiation and fight against tumor angiogenesis, as well as inhibit tumor invasion and metastasis. The present study aimed to investigate the anticancer effects of oxymatrine on nasopharyngeal cancer (NPC) cell death, and the underlying molecular mechanisms of these effects. NPC HK‑1 cells were incubated overnight and treated with oxymatrine (0, 2, 4, 6 and 8 mg/ml) for 1, 2 or 3 days. The results demonstrated that oxymatrine significantly inhibited NPC cell proliferation in a time‑ and dose‑dependent manner. Oxymatrine treatment also induced apoptosis, induced the activities of caspase‑3 and caspase‑9, promoted p53 and Bax protein expression, and suppressed cyclin D protein expression in these cells. The protein expression levels of phosphoinositide 3 kinase (PI3K), phosphorylated (p)‑AKT, p‑mammalian target of rapamycin, p‑p70 ribosomal protein S6 kinase and nuclear factor (NF)‑κB were significantly downregulated by oxymatrine treatment. In conclusion, results from the present study suggested that oxymatrine may induce NPC cell death through the inhibition of PI3K/AKT and NF‑κB signaling pathways.

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