Henan Provincial Cancer Hospital

Zhengzhou, China

Henan Provincial Cancer Hospital

Zhengzhou, China
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Zhang W.,Zhengzhou University | Liu D.,Henan Provincial Cancer Hospital | Ren J.,Zhengzhou University | Huang G.,Sun Yat Sen University | And 3 more authors.
International Journal of Clinical and Experimental Medicine | Year: 2017

The object of this study was to investigate the effects of interventional therapy with norcantharidin-loaded gelatin microspheres (NCTD/GMSs) via hepatic artery on hepatoma in mice. NCTD/GMSs were prepared by an emulsification-coacervation method. Tumor-bearing mice were divided into three groups and infused from the proper hepatic artery, which were control group receiving physiological saline, NCTD and NCTD/GMSs group. The concentration of the released NCTD was measured by UV-vis spectroscopy. Tumor volumes and weight were detected pre-injection and 1 to 5 weeks after NCTD/GMSs or NCTD treatment. MTT assay was used to detect the cell viability in HepG2 cells. Flow cytometry analysis was employed to measure apoptosis of HepG2 cells. Bcl-2, Bax, caspase-3 and caspase-9 levels were analyzed by Western blot. In vitro drug release kinetics indicated that there was an initial burst release followed by a slow and sustained release of NCTD from GMSs. The tumor volume of the mice in the NCTD/GMSs group was smaller than those in NCTD group and control group. Importantly, NCTD/GMSs promoted HepG2 cell death by triggering apoptosis and inhibited the ability of HepG2 cell invasion. In addition, NCTD/GMSs induced the reduction of Bcl-2 and increased Bax, caspase-3 and caspase-9 in HepG2 cells. Interventional therapy with NCTD/GMSs could yield preferable therapeutic effects on HCC in mice. This anti-tumor efficacy may be associated with the sustained releasing of NCTD. The mechanisms of NCTD antitumor effects seem to be mediated by inducing a caspase-3-dependent apoptosis. © 2017, E-Century Publishing Corporation. All rights reserved.


Sun Y.,Chinese Academy of Sciences | Wang J.W.,Chinese Academy of Sciences | Liu Y.Y.,Liaoning Provincial Cancer Hospital | Yu Q.T.,Guangxi Medical University | And 21 more authors.
Thoracic Cancer | Year: 2013

Background:: Phase II-III trials in patients with untreated and previously treated locally advanced or non-small cell lung cancer (NSCLC) suggested that Endostar was able to enhance the effect of platinum-based chemotherapy (NP regimen) with tolerable adverse effects. Methods: Four hundred and eighty six patients were randomized into two arms: study arm A: NP plus Endostar (n = 322; vinorelbine, cisplatin, Endostar), and study arm B: NP plus placebo (n = 164; vinorelbine, cisplatin, 0.9% sodium chloride). Patients were treated every third week for two to six cycles. Results:: Overall response rates were 35.4% in arm A and 19.5% in arm B (P = 0.0003). The median time to progression was 6.3 months for arm A and 3.6 months for B, respectively (P < 0.001). The clinical benefit rates were 73.3% in arm A and 64.0% in arm B (P = 0.035). Grade 3/4 neutropenia, anemia, and nausea/vomiting were 28.5%, 3.4%, and 8.0%, respectively, in Arm A compared with 28.2%, 3.0%, and 6.6%, respectively, in Arm B (P > 0.05). There were two treatment related deaths in arm A and one in arm B (P > 0.05). The median overall survival was longer in arm A than in arm B (P < 0.0001). Conclusion:: Long-term follow-up revealed that the addition of Endostar to an NP regimen can result in a significant clinical and survival benefit in advanced NSCLC patients, compared with NP alone. © 2013 Tianjin Lung Cancer Institute and Wiley Publishing Asia Pty Ltd.


Liu Y.,Henan Provincial Cancer Hospital | Xia Q.,Henan Provincial Cancer Hospital | Jia Y.,Henan Provincial Cancer Hospital | Guo H.,Henan Provincial Cancer Hospital | And 3 more authors.
Journal of Hematology and Oncology | Year: 2011

The role of thymidylate synthase (TS) is essential as a key rate-limiting enzyme in DNA synthesis. It is the primary target of fluorouracil and its derivates in colorectal cancer. In this study, TS mRNA expression was examined in primary tumor and normal tissues from 76 patients with high- risk stage II/III colorectal cancer by laser capture microdissection and polymerase chain reaction. Thirty (39.47%) patients were found to have higher TS expression in primary tumors with earlier stage (P = 0.018), lower histological grades (P = 0.001) and high frequency microsatellite instability (P = 0.000). Multivariate analysis showed that microsatellite instability, histological grade and number of lymph nodes examined are independent prognostic markers. © 2011 Liu et al; licensee BioMed Central Ltd.


Huang C.,Henan Provincial Cancer Hospital | Yu W.,Henan Provincial Cancer Hospital | Cui H.,Henan Provincial Cancer Hospital | Wang Y.,Henan Provincial Cancer Hospital | And 3 more authors.
Molecular Medicine Reports | Year: 2014

P2X7 is important in inflammation and tissue injury. The aim of the present study was to investigate the effect of P2X7 inhibition, using a specific inhibitor (A438079) to prevent the development of liver injury and fibrosis in a mouse model of liver fibrosis. The mouse liver fibrosis model was induced by carbon tetrachloride (CCl4). Mice received subcutaneous administration of vehicle (saline/olive oil), CCl4 or subcutaneous CCl4 and A438079. The pro-inflammatory and pro-fibrotic factors were determined by western blot analysis. The biochemistry, histopathology, collagen deposition and nuclear factor-κB (NF-κB) activity were also analyzed. Chronic CCl4 treatment resulted in liver injury and collagen accumulation. The expression levels of P2X7, pro-inflammatory and pro-fibrotic mediators, and the activity of NF-κB were markedly increased. Treatment with A438079 significantly inhibited CCl4-induced P2X7 expression, and attenuated CCl4-induced liver injury and the inflammatory response. P2X7 blockade also significantly reduced the formation of collagen in the liver and the expression of α-smooth muscle actin and transforming growth factor-β1. This study demonstrated that P2X7 inhibition attenuated liver injury and fibrosis in a mouse model. Thus, P2X7 is a potential novel therapeutic target for liver injury and fibrosis.


Liu Y.-Y.,Henan Provincial Cancer Hospital | Yao S.-N.,Henan Provincial Cancer Hospital | Yao S.-N.,Zhengzhou University | Zhao Y.,Henan Provincial Cancer Hospital | And 5 more authors.
Leukemia and Lymphoma | Year: 2010

The phosphatase and tensin homolog deleted on chromosome 10 (PTEN) and P53 tumor suppressors are among the most commonly inactivated or mutated genes in human cancers, whose pathways cross-talk and interact in a complementary mode. In order to understand their roles and relationship in diffuse large B-cell lymphoma (DLBCL), we examined their expression and evaluated their prognostic significance in 62 patients with DLBCL treated with standard chemotherapy. Results showed that PTEN protein was lost in 23 (37.1%) cases, and the loss was associated with the activation of PI3K/AKT pathway, but was not associated with patient's clinical outcome. P53 mutation protein was detected in 30 (48.4%) cases and was associated with poor survival. Results of multivariate analysis showed that P53 mutation but not PTEN loss is associated with short survival in patients with DLBCL. PTEN status has no effect on P53 mutation-associated poor survival. We conclude that PTEN may play less prognostic role than P53 and that P53 mutation protein should be considered as a predictive factor of the need for a more aggressive therapy in patients with DLBCL who express P53. © 2010 Informa UK, Ltd.


Zhu S.,Zhengzhou University | Gong G.,Zhengzhou University | Oremo J.A.,Zhengzhou University | Zhen M.,Zhengzhou University | And 3 more authors.
Information Technology Journal | Year: 2013

Analyzing Differential Expression Gene (DEG) and identifying candidate gene in prostate cancer cell lines that were resistant to docetaxel, which might be used for the purposes of screening targeted therapy. Gene expression pro?les of the tumors from docetaxel treated mice were performed using Agilent human whole genomic oligonucleotide microarrays. The microarray data were validated and the differential expression genes were analyzed using IPA software. The prostate cancer cell lines PCS and LNCaP were sensitive to docetaxel but VcaP and CWR22 were resistant to docetaxel cell lines. It indicated that some genes up-regulated or down-regulated in docetaxel resistant cell lines may be candidate genes for targeted therapy, after evaluating by Gene Expression Microarray and signal pathway. The significantiy up-regulated genes including Bcl-11 A, EPHA4 and CX3CL1 may be the potential candidates for further investigation in docetaxel-resistant tumor cells. © 2013 Asian Network for Scientific Information.


Zhang Y.,Henan Provincial Cancer Hospital
Chinese Journal of Clinical Oncology | Year: 2010

Objective: To study the clinical significance of serum soluble E-selectin (sE-selectin) in diagnosis and treatment of gastric cancer. Methods: Serum E-selectin was detected with ELISA in 200 cases of gastric cancer, 45 cases of benign gastric diseases and 40 healthy controls. The changes in serum sE-selectin level of 140 patients with gastric cancer were analyzed before and after surgery, and the positive ratio of sE-selectin was compared with that of CEA, CA199 and CA724 in patients with gastric cancer. Results: The level of serum sE-selectin in patients with gastric cancer was 69.12±18.19 ng/mL, higher than that in those with benign diseases [(19.47±7.88)ng/mL] and healthy controls [(15.85±5.27)ng/mL]. The differences were significant (P<0.01). The level of serum sE-selectin was correlated with clinical stage and hepatic metastasis in gastric cancer patients, but was not correlated with focal location and histological grade (P>0.05). The positive rate of serum sE-selectin in cases with hepatic metastasis was higher than that in those without hepatic metastasis (P<0.01). The level of serum sE-selectin in patients with gastric cancer declined significantly at one month after surgery. The positive rate of serum sE-selectin in patients with gastric cancer was much higher than that of other digestive tumor markers (CEA, CA199, and CA724, P<0.01). Conclusion: sE-selectin may be a valuable marker for early diagnosis and prognosis of gastric cancer.


Zou B.,University of Sichuan | Li T.,Sichuan Provincial Cancer Hospital | Zhou Q.,Suining Center Hospital | Ma D.,North Sichuan Medical College | And 14 more authors.
Medicine (United States) | Year: 2016

To evaluate the treatment pattern and survival of patients receiving radical resection for primary small cell carcinoma of the esophagus (PSCCE). This retrospective study included 150 patients who received radical resection of PSCCE. Data were retrieved from 4 centers in Western China. Thirty-nine of 150 patients received postoperative chemo-radiotherapy, 62 received postoperative chemotherapy, and 49 received radical resection only. The median radiation dosage was 50 Gy. The chemotherapeutic regimen was platinum-based and lasted for 2 to 6 cycles (median, 3). Median disease-free survival (mDFS) and overall survival (mOS) were 12.0 and 18.3 months, respectively. Subgroup analysis revealed that postoperative therapy did not improve survival in limited stage I (LSI) disease, whereas postoperative chemotherapy improved survival in limited stage II (LSII) disease. Relative to chemotherapy alone, chemoradiotherapy did not improve survival in patients with completely resected LSII disease. A multivariate analysis indicated an association of no postoperative chemotherapy with shorter DFS (P = 0.050) and OS (P = 0.010). Higher lymph node stage and length of disease longer than 3 cm were poor prognostic factors for both DFS and OS. Adjuvant chemotherapy improves survival in PSCCE patients with completely resected LSII disease. Adjuvant treatment with postoperative chemotherapy alone or postoperative chemo-radiotherapy does not increase survival in completely resected LSI disease. © Copyright 2016 Wolters Kluwer Health, Inc. All rights reserved.


PubMed | Henan Provincial Cancer Hospital
Type: Journal Article | Journal: Molecular medicine reports | Year: 2013

P2X7 is important in inflammation and tissue injury. The aim of the present study was to investigate the effect of P2X7 inhibition, using a specific inhibitor (A438079) to prevent the development of liver injury and fibrosis in a mouse model of liver fibrosis. The mouse liver fibrosis model was induced by carbon tetrachloride (CCl4). Mice received subcutaneous administration of vehicle (saline/olive oil), CCl4 or subcutaneous CCl4 and A438079. The proinflammatory and profibrotic factors were determined by western blot analysis. The biochemistry, histopathology, collagen deposition and nuclear factorB (NFB) activity were also analyzed. Chronic CCl4 treatment resulted in liver injury and collagen accumulation. The expression levels of P2X7, proinflammatory and profibrotic mediators, and the activity of NFB were markedly increased. Treatment with A438079 significantly inhibited CCl4induced P2X7 expression, and attenuated CCl4induced liver injury and the inflammatory response. P2X7 blockade also significantly reduced the formation of collagen in the liver and the expression of -smooth muscle actin and transforming growth factor1. This study demonstrated that P2X7 inhibition attenuated liver injury and fibrosis in a mouse model. Thus, P2X7 is a potential novel therapeutic target for liver injury and fibrosis.


PubMed | Henan Provincial Cancer Hospital
Type: Journal Article | Journal: Leukemia & lymphoma | Year: 2010

The phosphatase and tensin homolog deleted on chromosome 10 (PTEN) and P53 tumor suppressors are among the most commonly inactivated or mutated genes in human cancers, whose pathways cross-talk and interact in a complementary mode. In order to understand their roles and relationship in diffuse large B-cell lymphoma (DLBCL), we examined their expression and evaluated their prognostic significance in 62 patients with DLBCL treated with standard chemotherapy. Results showed that PTEN protein was lost in 23 (37.1%) cases, and the loss was associated with the activation of PI3K/AKT pathway, but was not associated with patients clinical outcome. P53 mutation protein was detected in 30 (48.4%) cases and was associated with poor survival. Results of multivariate analysis showed that P53 mutation but not PTEN loss is associated with short survival in patients with DLBCL. PTEN status has no effect on P53 mutation-associated poor survival. We conclude that PTEN may play less prognostic role than P53 and that P53 mutation protein should be considered as a predictive factor of the need for a more aggressive therapy in patients with DLBCL who express P53.

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