Patterns of failure after involved field radiotherapy for locally advanced esophageal squamous cell carcinoma.

PURPOSE: To retrospectively analyze the patterns of failure and the treatment effects of involved-field irradiation (IFI) on patients treated with locally advanced esophageal squamous cell carcinoma (ESCC) and to determine whether IFI is practicable in these patients. METHODS: A total of 79 patients with locally advanced ESCC underwent three dimensional conformal (3D)CRT) or intensity modulated radiotherapy (IMRT) using IFI or elective nodal irradiation (ENI) according to the target volume. The patterns of failure were defined as local/regional, in-field, out)of)field regional lymph node (LN) and distant failure. With a median follow)up of 32.0 months, failures were observed in 66 (83.6%) patients. RESULTS: The cumulative incidence of local/regional failure (55.8 vs 52.8%) and in)field regional lymph node failure (25.6 vs 19.4%) showed no statistically significant difference between the IFI and the ENI group (p=0.526 and 0.215, respectively). Out)of)field nodal relapse rate of only 7.0% was seen in the IFI group. Three)year survival rates for the ENI and IFI group were 22.2 and 18.6%, respectively (p=0.240), and 3)year distant metastasis rates were 27.8 and 32.6%, respectively (p=0.180). The lung V10, V20, V30 and mean lung dose of the ENI group were greater than those of the IFI group, while the mean lung dose and V10 had statistically significant difference. CONCLUSIONS: The patterns of failure and survival rates in the IFI group were similar as in the ENI group; the regional recurrence and distant metastasis are the main cause of treatment failure. IFI is feasible for locally advanced ESCC. Further investigation is needed to increase local control and decrease distant metastasis in these patients.

Inhibition of KiSS-1 on metastasis of nasopharyngeal carcinoma implant tumor in nude mice.

BACKGROUND: Nasopharyngeal carcinoma (NPC) is a kind of head-neck malignant neoplasm originated from the nasopharyngeal epithelium and is mainly prevalent in Southern China and Southeast Asia countries. KiSS-1 is an inhibitor of tumor metastasis in a range of cancers. METHODS: We establish a cell substrain of SUNE-1-5-8F (NPC cell line from humans) that trsnfected with lentiviral vectors carried with KiSS-1 gene and were selected by puromycin. A transplantation tumor animal model in BALB/c-nu mice was successfully established with a substrain that stably overexpressed KiSS-1. RESULTS: Our result showed that the size of transplantation tumor in the nude mice with KiSS-1 overexpression in transplantation tumor was not difference from the size of transplantation tumor in the controlled transplantation tumor mice. We detected metastatic tumor in lung but not in liver. Moreover, we also found that in the nude mice with KiSS-1 overexpression in transplantation tumor showed extremely fewer metastatic tumor in lung compared with the controlled transplantation tumor mice model. In conclusion, KiSS-1 may be beneficial for the inhibition of metastasis of human NPC. CONCLUSION: This study may throw light on the treatment of NPC and may help improve the prognosis of patients with NPC.

Targeted inhibition of Notch1 gene enhances the killing effects of paclitaxel on triple negative breast cancer cells.

OBJECTIVE: To study the influence of targeted inhibition of Notch1 gene on the killing effects of paclitaxel on triple negative breast cancer cells. METHODS: The triple negative [estrogen receptor (ER)/progesterone receptor (PR)/human epidermal growth factor receptor 2 (Her2)] breast cancer cell line MDA-MB-231 and ER/PR/HER-2-positive breast cancer cell line MCF-7 were cultured, transfected with Notch1-siRNA-overexpression plasmid and blank plasmid, and treated with different concentrations of paclitaxel, and then the cell proliferation activity and apoptosis rate as well as the mRNA expression of Caspase-3, Caspase-9 and Bcl-2 were determined. RESULTS: Paclitaxel could decrease the MDA-MB-231 and MCF-7 cell proliferation activity as well as Bcl-2 mRNA expression, and increase MDA-MB-231 and MCF-7 cell apoptosis rate as well as Caspase-3 and Caspase-9 mRNA expression in dose-dependent manners; with the same dose of paclitaxel treatment, the inhibitory effects on MDA-MB-231 cell proliferation activity and Bcl-2 mRNA expression as well as the promoting effects on MDA-MB-231 cell apoptosis and mRNA expression of Caspase-3 and Caspase-9 were weaker than those on MCF-7 cell; after 0.5 µM paclitaxel combined with Notch1-siRNA treatment, MDA-MB-231 cell proliferation activity and Bcl-2 mRNA expression were significantly lower than those after 0.5 µM paclitaxel combined with control plasmid treatment while cell apoptosis rate and mRNA expression of Caspase-3 and Caspase-9 were higher than those after 0.5 µM paclitaxel combined with control plasmid treatment. CONCLUSIONS: Targeted inhibition of Notch1 gene may enhance the killing effects of paclitaxel on triple negative breast cancer cells by up-regulating the expression of Caspase-3 and Caspase-9 and inhibiting the expression of Bcl-2.