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Nanchang, China

Zeng S.,Jiangxi Maternal and Child Health Hospital | Li L.,Jiangxi Maternal and Child Health Hospital | Zhong M.,Jiangxi Maternal and Child Health Hospital | Jiang W.,Jiangxi Maternal and Child Health Hospital | Xiao Y.,Jiangxi Tumor Hospital
Chinese-German Journal of Clinical Oncology | Year: 2012

Objective: The aim of the study was to compare the efficacy, side effect and influence on the survival rate of two chemotherapy regimens, paclitaxel liposome combined with platinum and paclitaxel combined with platinum, in concurrent chemoradiotherapy for cervical carcinoma. Methods: The 162 cases with primary cervical carcinoma diagnosed between January 2008 and November 2009 in Jiangxi Maternal and Child Health Hospital (China) were enrolled in this randomized controlled trial. Seventy-one cases were included in paclitaxel group and 91 in paclitaxel liposome group. And the chemotherapy doses were as follows: paclitaxel liposome and paclitaxel 135 mg/m 2; cisplatin 80 mg/m 2 or carboplatin AUC 4-6; then repeated every 21 days for two or three times. Radical radiotherapy was given to both groups at the same time. Efficacy was evaluated according to the tumor regression six months later and follow-up was done consistently. Results: The overall response rates of paclitaxel group and paclitaxel liposome group were 90.1% and 89 % respectively (P > 0.05). The one year cumulative survival was 91.4% for paclitaxel group and 89.2% for paclitaxel liposome group (P > 0.05). The incidence rates of adverse effects such as rash, gastrointestinal toxicity, bone marrow suppression and muscle/joint pain in paclitaxel liposome group were much lower than those in paclitaxel group (P < 0.05), while there was no difference regarding hair loss, hepatic function damage, peripheral neuritis and other aspects (P > 0.05). Conclusion: Paclitaxel liposome plus platinum is a safe and effective method for staging IIa-IV cervical carcinomas. While the long-term efficacy should be further observed. © Huazhong University of Science and Technology and Springer-Verlag Berlin Heidelberg 2012. Source


Yang X.,Jiangxi Tumor Hospital | Zhang Y.,CAS Wuhan Institute of Hydrobiology | Zhang Y.,CAS Wuhan Institute of Virology | Zhang L.,Nanjing Southeast University | And 3 more authors.
Acta Biochimica et Biophysica Sinica | Year: 2014

The normal cellular prion protein, PrPC is a highly conserved and widely expressed cell surface glycoprotein in all mammals. The expression of PrP is pivotal in the pathogenesis of prion diseases; however, the normal physiological functions of PrPC remain incompletely understood. Based on the studies in cell models, a plethora of functions have been attributed to PrPC. In this paper, we reviewed the potential roles that PrP C plays in cell physiology and focused on its contribution to tumorigenesis. © 2014 The Author 2014. Source


Gao Z.,University of Chinese Academy of Sciences | Gao Z.,Wuhan University | Zhang H.,University of Chinese Academy of Sciences | Hu F.,Wuhan Brain Hospital | And 6 more authors.
Cellular Signalling | Year: 2016

Whether the two N-linked glycans are important in prion, PrP, biology is unresolved. In Chinese hamster ovary (CHO) cells, the two glycans are clearly not important in the cell surface expression of transfected human PrP. Compared to fully-glycosylated PrP, glycan-deficient PrP preferentially partitions to lipid raft. In CHO cells glycan-deficient PrP also interacts with glycosaminoglycan (GAG) and vascular endothelial growth factor receptor 2 (VEGFR2), resulting in VEGFR2 activation and enhanced Akt phosphorylation. Accordingly, CHO cells expressing glycan-deficient PrP lacking the GAG binding motif or cells treated with heparinase to remove GAG show diminished Akt signaling. Being in lipid raft is critical, chimeric glycan-deficient PrP with CD4 transmembrane and cytoplasmic domains is absent in lipid raft and does not activate Akt signaling. CHO cells bearing glycan-deficient PrP also exhibit enhanced cellular adhesion and migration. Based on these findings, we propose a model in which glycan-deficient PrP, GAG, and VEGFR2 interact, activating VEGFR2 and resulting in changes in cellular behavior. © 2016 Elsevier Inc.. Source


Zhang R.,Jiangxi University of Traditional Chinese Medicine | Liu J.-Q.,Jiangxi University of Traditional Chinese Medicine | Liu L.-Y.,Jiangxi Tumor Hospital | Xue P.,Jiangxi University of Traditional Chinese Medicine
Chinese Traditional and Herbal Drugs | Year: 2010

Objective: To establish a separation method of tricin reference substance from Bambusa textilis. Methods: After extracted with ethyl acetate, the extract of B. textilis was isolated and purified by silica gel column chromatography and preparative HPLC. Tricins were identified by melting point, UV, and IR spectroscopy. Results: The content of tricin was over 98% by normalization method of HPLC. Conclusion: The developed method is simple with lower cost, by which tricin can be used as reference substances for the qualitative and quantitative analyses of Chinese herbal medicine. Source


Gan X.,Jiangxi Provincial Peoples Hospital | Liu Z.,Jiangxi Tumor Hospital | Tong B.,Nanchang University | Zhou J.,Jiangxi Tumor Hospital
Tumor Biology | Year: 2015

Integrin, beta-like 1 (ITGBL1), is a β-integrin-related extracellular matrix protein which contains ten EGF-like repeats domain. Surprisingly, we screen Oncomine Database and found that ITGBL1 is more commonly downregulated in non-small cell lung cancer (NSCLC) tissues, and the result reminds us to explore its significance in NSCLC. Thus, we retrieved DRUGSURV Database and found that downregulated ITGBL1 predicts a poor prognosis of patients. These results provided us the clues that ITGBL1 might be a tumor suppressor in NSCLC. However, the biological functions of ITGBL1 have not been reported to date. In the current study, we surprisingly found that knockdown of ITGBL1 in NSCLC cell lines could promote cancer cell migration and invasion. Furthermore, recombinant ITGBL1 protein-treated cancer cell could inhibit cell migration and invasion. These results suggested that ITGBL1 plays a suppressive role in NSCLC progression. We further found that the downregulation of ITGBL1 might result from highly expressed miR-576-5p in NSCLC tissues, and the activity of Wnt/PCP signaling was enhanced when the level of ITGBL1 was inhibited. In conclusion, our results suggest that ITGBL1 is a novel tumor suppressor in NSCLC progression. © 2015 International Society of Oncology and BioMarkers (ISOBM) Source

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