RESUMEN
The crystal structure of the title compound in the paper by Sui, Fang, Luo, Chen & Zhou [Acta Cryst. (2006), E62, m1994-m1996] has been rerefined to allow for identification of a disordered dimethyl sulfoxide ligand.[This corrects the article DOI: 10.1107/S1600536806028832.].
RESUMEN
PURPOSE: Anlotinib is a newly developed oral multitarget tyrosine kinase inhibitor. We retrospectively evaluated the toxicity and clinical efficacy of chemotherapy combined with anlotinib versus chemotherapy alone for metastatic/advanced non-small cell lung cancer (NSCLC) in patients who failed first- or second-line systemic treatment in China. PATIENTS AND METHODS: In this retrospective trial, ninety-four advanced NSCLC patients received chemotherapy combined with anlotinib (n = 41) or chemotherapy alone (n = 53) in Henan Cancer Hospital. We recorded the objective response rate (ORR), disease control rate (DCR), progression-free survival (PFS) and adverse events (AEs). RESULTS: In the anlotinib plus chemotherapy group, eleven patients (27%) achieved a PR (partial response), and twenty-one patients (51%) achieved SD (stable disease), with an ORR of 27% and a DCR of 78%. In the chemotherapy alone group, eight patients (15%) achieved a PR, and nineteen patients (36%) had SD, with an ORR of 15% and a DCR of 51%. The ORR in the combination arm was slightly, but not obviously, higher than that in the chemotherapy arm (27% vs 15%, p > 0.05). In addition, the DCR was significantly higher in the combination arm than in the chemotherapy alone arm (78% vs 51%, p=0.007). At the end of follow-up, patients in the combination arm had a 1.5-month longer median PFS than patients in the chemotherapy arm; this difference was statistically significant (5.0 vs 3.5, p=0.002). The median OS was not achieved at the final analysis. The hematological and nonhematological toxicities were well tolerated and controlled. In general, most toxicity was limited to grade I or II, well tolerated and controlled. CONCLUSION: Our study suggests that anlotinib combined with chemotherapy may be an effective and well-tolerated treatment for advanced NSCLC in patients who fail first- or second-line therapy.
RESUMEN
OBJECTIVE: To study the anti-tumor effect of Tetrandrine (Tet) combined with Nedaplatin (Nap) on the human liver cancer cell line 7402, and explore its mechanism. METHODS: Human liver cancer line 7402 was treated by Tet and Nap in various concentrations respectively or in combination in vitro,and then the cell growth was assayed by MTT method, periodic return changes were observed by aridine orange (AO)-/ethidiumbromide (EB) fluorescent staining, DNA gel eledtophoresis and flow cytometry, and the expression of apoptosis-related genes were analyzed by immunohistochemical staining method. RESULTS: Compared with Tet or Nap individual drug groups, Tet combined with Nap obviously increased the inhibitatory rate and apoptosis rate of the human liver cancer cell line 7402. The cell cycle distribution was altered and ratio of S phase and G2/M phase cell increased following the treatment with Tet combined with Nap, with Bcl-2 gene expression down-regulated, and BAX gene expression up-regulated. CONCLUSION: Tet combined with Nap can obviously increase apoptosis-inducing effect, and its mechanism may be regulating cell cycle and increasing apoptosis-inducing effect which is regulated by several genes.