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Zhuang Y.,Shanghai JiaoTong University | Jiang L.,Shanghai JiaoTong University | Zhao Y.,Shanghai JiaoTong University | Qian J.,Shanghai JiaoTong University | Gao X.,Central Hospital of Shanghai Minhang District
Chinese Journal of Lung Cancer | Year: 2015

Background and objective Most small cell lung cancer (SCLC) patients relapse or progress and have low survival rate although they have significant response to initial chemotherapy and radiotherapy. This study intends to explore the factors affecting the relapse (or progression) of nonoperative SCLC and to explore the correlations between progressionfree survival (PFS) and overall survival (OS). Methods Clinical data of 182 patients diagnosed with SCLC between January 2009 and December 2011 at Shanghai Chest Hospital has been reviewed and retrospectively analyzed. All of these patients accepted chemotherapy combined (or not combined) with radiotherapy, and relapsed or progressed after first-line therapy. Univariate Kaplan-Meier survival estimates as well as multivariate Cox regression survival analysis were used to locate the potential factors affecting PFS. The correlation between PFS and OS was analyzed via Bivariate Correlation Analysis method. Results The univariate estimates showed that the TNM stage, liver metastasis or not, brain metastasis or not, first-line chemotherapy cycles, effect of initial chemotherapy, and thoracic radiotherapy combined or not were the significant contributive factors to PFS. In the subgroup of the patients without brain metastases, those received prophylactic cranial irradiation (PCI) had longer PFS. Cox regression indicated that the three independent variables of first-line chemotherapy cycles, effect of initial chemotherapy and thoracic radiotherapy combined or not were closely related to PFS. In addition, significant positive correlation between PFS and OS had been observed. Conclusion PFS could be prolonged by having more first-line chemotherapy cycles (>4 cycles), obtaining better effect of initial chemotherapy (partial response or complete response), combining with thoracic radiotherapy and implementing PCI for patients without brain metastasis. © 2015, Chinese Journal of Lung Cancer. All rights reserved. Source


Shi R.,Central Hospital of Shanghai Minhang District | Liu W.,Central Hospital of Shanghai Minhang District | Liu B.,Shanghai JiaoTong University | Xu Z.,Central Hospital of Shanghai Minhang District | And 2 more authors.
Oncology Reports | Year: 2013

Gastric cancer is the fourth most common cancer worldwide. Several signaling pathways are involved in gastric cancer development and progression. Slit2 was recently found to be involved in cancer; however, its expression pattern in gastric cancer has not been discovered yet. In the present study, we investigated the expression of Slit2 in human gastric cancer and its correlation with the expression and subcellular localization of β-catenin. Immunohistochemistry (IHC) staining revealed that Slit2 was highly expressed in human gastric cancer tissues, while it was low or weakly expressed in normal gastric tissues. The differences in clinicopathological features between different groups were determined using Pearson's χ2 test. Slit2 levels were significantly associated with differentiation, Lauren's classification, lymph node metastasis and TNM staging. Slit2 levels were positively correlated with β-catenin level in gastric cancer tissues and cell lines. High levels of Slit2 were correlated with the membrane localization of β-catenin, and low levels of Slit2 were correlated with nuclear translocation of β-catenin in both gastric cancer tissues and cell lines assayed by IHC and immunofluorescence staining, respectively. Our data suggest that Slit2 was highly expressed in gastric cancer patients with less advanced clinicopathological features. Slit2 levels were correlated with β-catenin level and subcellular localization. Source


Shi R.,Central Hospital of Shanghai Minhang District | Yang Z.,Central Hospital of Shanghai Minhang District | Liu W.,Central Hospital of Shanghai Minhang District | Liu B.,Shanghai JiaoTong University | And 2 more authors.
Oncology Reports | Year: 2014

We previously showed that Slit2 was highly expressed in gastric cancer tissues that exhibit less advanced clinicopathological features, suggesting a tumor suppressor role for Slit2. In the present study, we investigated the effects of Slit2 knockdown on gastric cancer cells. Slit2-specific shRNAs were used to generate Slit2-knockdown SGC-7901 gastric cancer cells. Cell proliferation assay, Annexin V/PI double staining and cell cycle analysis were used to investigate the role of Slit2 knockdown in cell growth. Wound-healing and in vitro migration/invasion assays were performed. Subcutaneous tumor formation and peritoneal spreading in nude mice were employed to examine the in vivo effects of Slit2 knockdown. Cell signaling changes induced by Slit2 knockdown were analyzed by immunoblotting. Slit2 knockdown increased gastric cancer cell growth in monolayer and soft agar/Matrigel 3D culture. Slit2 knockdown inhibited apoptosis but did not alter cell cycle progression. Slit2-knockdown cells formed larger tumors and produced more peritoneal metastatic nodules in nude mice. Slit2 knockdown increased AKT phosphorylation, activated anti-apoptotic signaling, suppressed GSK3β activity and induced β-catenin activation. Blocking the effects of PI3K/AKT using pharmacological inhibitors abolished the ability of Slit2 knockdown to induce apoptosis resistance and cell migration/invasion. These results indicate that Slit2 knockdown promotes gastric cancer growth and metastasis through activation of the AKT/β-catenin-mediated signaling pathway. Source


Li C.-X.,Shanghai JiaoTong University | Mao Y.-Q.,Shanghai JiaoTong University | Gao Y.-H.,Central Hospital of Shanghai Minhang District | Han S.-F.,Central Hospital of Shanghai Minhang District | And 2 more authors.
Journal of Shanghai Jiaotong University (Medical Science) | Year: 2014

Objective: To observe the effects of tumor suppressor gene VHL on the H2O2 induced oxidative stress of tumor cells and to primarily explore the molecular mechanism. Methods: The expressions of vhl-1 gene of C.elegans and homologous gene VHL of cancer cells were silenced by RNAi. The death of C.elegans was morphologically analyzed after being treated by H2O2 of different concentrations. Cells were labeled by Annexin V and PI and the death of cells was analyzed by the flow cytometry. Then the phosphorylation level of pathway protein c-Jun N-terminal kinase (JNK) of oxidative stress was detected by the Western blotting and the molecular mechanism of effects of VHL on the oxidative stress of cells was analyzed. Results: Compared to the control group, the sensitivity of C.elegans with silenced VHL gene towards H2O2 increased significantly and the mortality rate also increased significantly. These effects depended on the concentration gradient and treatment time of H2O2. The mortality rate of tumor cells with silenced VHL gene was not significantly different from that of wild type tumor cells. But the mortality rate of tumor cells with silenced VHL gene significantly increased and the phosphorylation level of JNK also increased after being treated by H2O2 of 250 μmol/L and 500 μmol/L. Conclusion: Silencing the expression of VHL can increase the sensitivity of cells towards the oxidative stress induced by H2O2. The protective effect of VHL on the H2O2 induced oxidative stress is conserved in species. ©, 2014, Editorial Department of Journal of Shanghai Second Medical University. All right reserved. Source

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