Hunan Provincial Tumor Hospital

Changsha, China

Hunan Provincial Tumor Hospital

Changsha, China
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He X.,Central South University | Ou P.,Central South University | Wu K.,Central South University | Huang C.,Central South University | And 3 more authors.
Neuroscience Letters | Year: 2014

In recent years, researchers have begun to pay more attention to the role of Sirtuin 1 (SIRT1, a class III histone deacetylase) in pain. However, little research has been conducted examining the involvement of SIRT1 in chronic morphine tolerance. The aim of this study was to investigate the role of spinal SIRT1 and acetyl-histone H3(Ac-H3) in chronic morphine tolerance in rats. Chronic morphine tolerance was induced by twice-daily intrathecal (i.t.) injections of morphine (10. μg) for 6 days. Control rats received normal saline (NS). Resveratrol (Res, a SIRT1 stimulant, 30. μg i.t.) or dimethyl sulfoxide (DMSO, 10. μl i.t.) was then injected on days 7-13. The thermal paw withdrawal threshold was assessed to determine the analgesic effects of morphine (10. μg). qRT-PCR, western blotting and immunohistochemistry were used to detect the expression of SIRT1 and global Ac-H3. Administration of morphine for 6 days induced a stabilized antinociceptive tolerance, down-regulated SIRT1 expression and up-regulated Ac-H3 expression in the spinal dorsal horn. Resveratrol treatment from day 7 to 13 increased SIRT1 expression, suppressed global Ac-H3 expression compared to the morphine tolerance (MT) group, and significantly reversed morphine antinociceptive tolerance. These results suggest that resveratrol reversed morphine tolerance by upregulating the expression of SIRT1 in the spinal dorsal horn. SIRT1 and global Ac-H3 in the spinal cord may play an important role in the mechanisms of chronic morphine tolerance. © 2014 Elsevier Ireland Ltd.


Zhao Y.,PLA Fourth Military Medical University | Wang W.J.,PLA Fourth Military Medical University | Guan S.,Zhengzhou University | Li H.L.,Henan Tumor Hospital | And 10 more authors.
Annals of Oncology | Year: 2013

Background: Data on the efficacy and safety of sorafenib in combination with transarterial chemoembolization (TACE) in patients with advanced hepatocellular carcinoma (HCC) are lacking. Patients and methods: In this multicenter retrospective study, 222 consecutive HCC patients receiving combination therapy were enrolled between June 2008 and July 2011. Results: Chronic hepatitis B was the predominant cause of HCC (86%). Eighty percent patients were at Barcelona Clinic Liver Cancer (BCLC) stage C, and 86% patients were in Child-Pugh (CP) A class. The overall median survival was 12 months (95% CI 10.1-13.9). The overall incidence of adverse events (AEs) was 87%. In 177 BCLC-C patients, performance status, the number of HCC nodules, Child-Pugh score and macrovascular invasion were significantly associated with overall survival (OS) and were included in the final risk scores (R), where R = 5 × (vascular invasion: 0 if no, 1 yes) + 6 × (CP: 0 if A, 1 if B) + 7 × (no. of lesions: 0 if 1-2, 1 =3) + 8 × (Eastern Cooperative Oncology Group, ECOG: 0 if 0, 1 =1). Conclusions: Sorafenib in combination with TACE should be considered a safe and effective therapy for advanced HCC. Further validation of the new subgroup of BCLC-C stage is warranted in an independent patient cohort. © The Author 2013. Published by Oxford University Press on behalf of the European Society for Medical Oncology. All rights reserved.


Feng X.,Chongqing Medical University | Xu R.,Hunan Provincial Tumor Hospital | Du X.,PLA Fourth Military Medical University | Dou K.,Xijing University | And 9 more authors.
American Journal of Gastroenterology | Year: 2014

OBJECTIVES:The objective of this study was to evaluate the efficacy of combined therapy using Sorafenib and radiofrequency ablation (RFA) with curative intent for all detectable lesions in patients with Barcelona Clinic Liver Cancer (BCLC) Stage 0-B1 hepatocellular carcinoma (HCC).METHODS:One hundred and twenty-eight patients with HCC from 12 centers were enrolled in this retrospective study; 64 patients who received Sorafenib plus RFA (Sorafenib-RFA) were compared with a control group treated with RFA alone. The two patient groups were selected with a predefined criterion and matched in terms of their clinical and tumor characteristics at baseline. The primary end point of the study was the incidence of post-RFA HCC recurrence. Secondary end points were overall survival (OS) and treatment toxicity.RESULTS:During a median follow-up of 134.1 weeks, 49 patients died and 79 survived. The 1-, 2-, and 3-year cumulative incidences of post-RFA recurrence were 40.5%, 62.9%, and 74.5%, respectively, in the Sorafenib-RFA group, and 62.8%, 85.4%, and 92.7%, respectively, in the RFA group. The 1-, 2-, 3-, and 4-year OS rates were 85.6%, 64.0%, 58.7%, and 50.3%, respectively, in the Sorafenib-RFA group, and 80.7%, 47.2%, 30.9%, and 30.9%, respectively, in the RFA group. Thus, the Sorafenib-RFA group exhibited better survival than the RFA alone group.CONCLUSIONS:Combined therapy with Sorafenib-RFA was associated with a lower incidence of post-RFA recurrence and better OS than RFA alone in patients with BCLC Stage 0-B1 HCC. Although these findings suggest that Sorafenib and RFA is safe and effective for the treatment of early HCC, prospective and randomized controlled trials are needed to validate them. © 2014 by the American College of Gastroenterology.


Li X.,Foshan University | Xu Q.,Thomas Jefferson University | Wu Y.,Central South University | Li J.,Hunan provincial Tumor Hospital | And 3 more authors.
Carcinogenesis | Year: 2014

Cancer-associated fibroblasts (CAFs) have been described to play critical roles in initiation, progression and metastasis of various cancers. However, the involvement of CAFs in oral cancer (OC) has not been well addressed. In this study, we demonstrate that CAFs, when cocultured with OC cells (OCCs), produce high levels of chemokine (C-C motif) ligand 2 (CCL2) and, subsequently, enhance endogenous reactive oxygen species production in cells. Oxidative stress stimulates expression of cell cycle progression proteins in OCCs, leading to promotion of OCC proliferation, migration, invasion and, OC tumor growth. On the other hand, oxidative stress triggered the activation of nuclear factor-kappaB (NF-κB) and STAT3 in CAFs, resulting in accelerating CCL2 expression. In this way, CAFs-OCCs coculture creates a favorable cytokine-rich microenvironment, beneficial for both CAFs and OCCs. In addition, upregulation of CCL2 expression has been observed in oral squamous cell carcinoma tumors and patient plasma. We also showed that inhibition of CCL2 reduced OC tumor burden in mice. Therefore, our data suggested that CCL2 represents a potential therapeutic target for treatment of OC. © The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.


Zhang Z.,Hunan University | Yang C.,Hunan University | Gao W.,Hunan University | Chen T.,Hunan University | And 3 more authors.
Cancer Letters | Year: 2015

The Forkhead Box A2 (FOXA2) transcription factor is required for embryonic development and for normal functions of multiple adult tissues, in which the maintained expression of FOXA2 is usually related to preventing the progression of malignant transformation. In this study, we found that FOXA2 prevented the epithelial to mesenchymal transition (EMT) in human breast cancer. We observed a strong correlation between the expression levels of FOXA2 and the epithelial phenotype. Knockdown of FOXA2 promoted the mesenchymal phenotype, whereas stable overexpression of FOXA2 attenuated EMT in breast cancer cells. FOXA2 was found to endogenously bind to and stimulate the promoter of E-cadherin that is crucial for epithelial phenotype of the tumor cells. Meanwhile, FOXA2 prevented EMT of breast cancer cells by repressing the expression of EMT-related transcription factor ZEB2 through recruiting a transcriptional corepressor TLE3 to the ZEB2 promoter. The stable overexpression of FOXA2 abolished metastasis of breast cancer cells in vivo. This study confirmed that FOXA2 inhibited EMT in breast cancer cells by regulating the transcription of EMT-related genes such as E-cadherin and ZEB2. © 2015 Elsevier Ireland Ltd.


Qi S.,Shenzhen University | Ouyang X.,Jinan University | Wang L.,Hunan Provincial Tumor Hospital | Peng W.,Jinan University | And 2 more authors.
Clinical and Translational Science | Year: 2012

Background: Chronic kidney disease (CKD) is the end point of a number of renal and systemic diseases. The metabolomics with a highly multiplexed and efficient manner is a challenging goal in nephrology. Methods: A 1H-NMR based metabolomics approach was applied to establish a human CKD serum metabolic profile. Serum samples were obtained from CKD patients with four stages (N= 80) and healthy controls (N= 28). The data acquired by CMPG spectrum were further processed by pattern recognition (PR) analysis. Principal components analysis (PCA) and partial least-squares-discriminant analysis (PLS-DA) was capable of clustering the disease groups and establishing disease-specific metabolites profile. Results: The classification models could grade CKD patients with considerably high value of Q2 and R2. The significant endogenous metabolites that contributed to distinguish CKD in different stages included the products of glycolysis (glucose, lactate), amino acids (valine, alanine, glutamate, glycine), organic osmolytes (betaine, myo-inositol, taurine, glycerophosphcholine), and so on. Based on these metabolites, the model for diagnosing patients with CKD achieved the sensitivity and specificity of 100%. Conclusion: The study illustrated that serum metabolic profile was altered in response to renal dysfunction and the progression of CKD. The identified metabolic biomarkers may provide useful information for the diagnosis of CKD, especially in early stages. © 2012 Wiley Periodicals, Inc.


Huang G.W.,Central South University | Ding X.,Central South University | Chen S.L.,Hunan Provincial Tumor Hospital | Zeng L.,Hunan Provincial Tumor Hospital
Journal of Cancer Research and Clinical Oncology | Year: 2011

Purpose: To investigate the expression of claudin 10 in hepatocellular carcinoma (HCC) and the impact on angiogenesis and the postoperative survival of HCC patients. Methods: The expression of claudin 10 protein was analyzed on samples from 99 HCC patients undergoing hepatectomy with immunohistochemistry and 31 fresh specimens with Western blotting. We examined the relationship between claudin 10 expression with clinicopathological factors, microvessel density (MVD), and postoperative survival. Results: Western blotting and immunohistochemical staining showed that claudin 10 protein was highly expressed in HCC, compared with paraneoplastic liver tissue and normal liver tissue (P < 0.01). Claudin 10 protein expression levels were significantly higher in HCC specimens with microscopic venous invasion (P < 0.01). MVD in HCC increased with enhanced claudin 10 expression (P < 0.01). Kaplan-Meier survival analysis revealed that HCC patients with high claudin 10 expression had significantly shorter overall survival (P = 0.01). Multivariate analysis showed that claudin 10 expression was an independent prognostic indicator for postoperative overall survival of HCC patients (P < 0.01). Conclusions: Claudin 10 protein is highly expressed in HCC tissue and is closely related to angiogenesis. Claudin 10 protein could be a useful marker to predict poor prognosis of HCC patients after hepatectomy. © 2011 Springer-Verlag.


Zhu J.,Central South University | Luo C.,Central South University | Wang P.,Hunan Provincial Tumor Hospital | He Q.,Central South University | And 2 more authors.
Experimental and Therapeutic Medicine | Year: 2013

Saikosaponin A (SSA) is a major triterpenoid saponin isolated from Radix bupleuri (RB), a widely used Chinese traditional medicine to treat various inflammation-related diseases. The aim of this study was to investigate the anti-inflammatory activity, as well as the molecular mechanism of SSA in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. In this study, we demonstrated that SSA markedly inhibits the expression of certain immune-related cytotoxic factors, including cyclooxygenase-2 (COX-2) and inducible nitric-oxide synthase (iNOS), as well as pro-inflammatory cytokines, including tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6. It also significantly upregulates the expression of IL-10, an important anti-inflammatory cytokine, suggesting its anti-inflammatory activity in LPS-stimulated macrophages. We further demonstrated that SSA inhibits the activation of the nuclear factor-κB (NF-κB) signaling pathway by suppressing the phosphorylation of inhibitory NF-κB inhibitor α (IκBα) and thus holding p65 NF-κB in the cytoplasm to prevent its translocation to the nucleus. In addition, SSA also inhibits the mitogen-activated protein kinase (MAPK) signaling pathway by downregulating the phosphorylation of p38 MAPK, c-Jun N-terminal kinase (c-JNK) and extracellular signal-regulated kinase (ERK), the three key components of the MAPK family. In conclusion, our study demonstrates that SSA has an anti-inflammatory effect by regulating inflammatory mediators and suppressing the MAPK and NF-κB signaling pathways in LPS-stimulated RAW 264.7 cells.


Tang J.,Hunan Provincial Tumor Hospital | Tang Y.,Hunan Provincial Tumor Hospital | Yang J.,Hunan Provincial Tumor Hospital | Huang S.,Hunan Provincial Tumor Hospital
Gynecologic Oncology | Year: 2012

Purpose: The optimal treatment of women with advanced adenocarcinoma of uterine cervix is still undefined. We compared concurrent chemoradiation (CCRT) and adjuvant cisplatin-based chemotherapy with CCRT alone for advanced cervical adenocarcinoma in a randomized trial at the Hunan Provincial Tumor Hospital in China. Methods: From 1998 to 2007, 880 patients with clinical FIGO stages IIB-IVA cervical adenocarcinoma were randomized to receive either CCRT or chemoradiation with one cycle of neo-adjuvant chemotherapy with Paclitaxel (135 mg/m 2) + Cisplatin (75 mg/m 2) before receiving radiation and two cycles of consolidation chemotherapy with the same drugs after radiotherapy in 3-week intervals. The disease control and survival rates were calculated using the Kaplan-Meier method. Results: All patients completed the treatment plan. 340 patients have relapsed, with a median follow-up duration of 60 months. Patients who received chemoradiation with adjuvant chemotherapy showed a significantly longer disease-free (P < .05), cumulative survival (P < .05) and long-term local tumor control (P < .05). Patients who received CCRT alone had significantly more distant metastasis and pelvic failure than those who received chemoradiation with adjuvant chemotherapy (P < .05). Conclusion: Incorporating neo-adjuvant and consolidation chemotherapy with Paclitaxel and Cisplatin into concomitant chemoradiation is highly effective, safe and may be a very promising treatment protocol for advanced cervical adenocarcinoma. © 2012 Elsevier B.V. All rights reserved.


Patent
Hunan Provincial Tumor Hospital | Date: 2015-04-01

A human hepatoma cell line is HLCZ01 cell line which has been deposited in the China Center for Type Culture Collection (CCTCC), and having Accession (deposit) No. is CCTCC NO: C201309. The human hepatoma cell line HLCZ01 is used as a cell model supporting said hepatitis viruses infection and is used to establish an animal model for supporting virus infection, wherein said human hepatoma cell line HLCZ01 is also used for preparation, screening and evaluating anti-hepatitis virus drugs, anti-tumor drugs, and used for manufacturing artificial liver.

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