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We performed a phase II trial of docetaxel in combination with capecitabine to evaluate the antitumor response, toxicity, and survival in pre-treated patients with advanced esophageal squamous cell carcinoma. Patients with advanced esophageal squamous cell carcinoma who had failed first-line chemotherapy with cisplatin and 5-fluorouracil were enrolled in this study. Treatment consisted of oral capecitabine (825 mg/m2 twice daily on days 1–14) plus 1-h intravenous docetaxel (60 mg/m2 on day 1) every 3 weeks for up to 6 cycles. Between June 2008 and August 2011, thirty eligible patients with a median age of 58 years (range 38–68 years) were enrolled. Patients received a median of three cycles of treatment (range 1–6). The median follow-up was 15.4 months (range 1.0–31.5 months). Intent-to-treat efficacy analysis demonstrated an overall response rate of 23.3 % (0 complete response and 7 partial response) and stable disease of 43.4 % (n = 13). The median time to progression was 3.0 months (95 % CI 1.9–4.1 months). The median survival was 8.3 months (95 % CI 6.8–9.8 months). Severe adverse events (grade 3/4) reported were as follows: neutropenia (33.3 %, n = 10, including febrile neutropenia 6.7 %, n = 2), anemia (16.7 %, n = 5), thrombocytopenia (10 %, n = 3), hand–foot syndrome (13.3 %, n = 4), and fatigue (10 %, n = 3). Docetaxel plus capecitabine had a manageable adverse event profile and promising activity in advance esophageal squamous cell carcinoma as a second-line treatment.

We investigated the apoptosis-inducing effect of zoledronic acid in human nasopharyngeal carcinoma cell HNE-1 and explore the potential mechanism. Human nasopharyngeal carcinoma cell HNE-1 was exposed to various concentrations (0–40 μmol/L) of zoledronic acid. Cell proliferation was studied by an MTT assay. Cell apoptosis was analyzed by flow cytometry and TdT-mediated dUTP nick-end labeling (TUNEL) assay. Cell cycle was analyzed by flow cytometry. Gene expressions were investigated by quantitative real-time PCR, and protein expressions were investigated by Western blot. The results showed zoledronic acid decreased cell proliferation not in a time- or dose-dependent fashion. TUNEL assay, together with Annexin V/propidium iodide FACS analysis, confirmed the increase in apoptotic HNE-1 cells treated with zoledronic acid. Cell cycle analysis showed a larger number of treated cells occupied the S-phase. Quantitative RT-PCR and Western blot revealed that the pro-apoptotic genes, Bad, Bax, and Caspase-9, were upregulated in treated HNE-1 cells, whereas the anti-apoptotic gene, Bcl-2, was downregulated in both mRNA and protein levels. In conclusion, zoledronic inhibits human nasopharyngeal carcinoma cell proliferation by inducing apoptosis via the mitochondrial apoptotic pathway.