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Pancreatic Neoplasms: HELP
Articles by C. Huang
Based on 6 articles published since 2010
(Why 6 articles?)
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Between 2010 and 2020, C. Huang wrote the following 6 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article [Diagnostic value and patient compliance of a pancreas-oriented multidisciplinary clinic: a retrospective analysis from a Chinese pancreatic disease center]. 2019

Li, J A / Wu, W C / Ji, Y / Liu, L X / Rao, S X / Wang, D S / Zhang, Y Q / Yao, X Z / Fan, Y / Huang, C / Zhou, Y H / Lou, W H. ·Department of Pancreatic Surgery, Zhongshan Hospital Fudan University, Shanghai 200032, China. · Department of Pathology, Zhongshan Hospital Fudan University, Shanghai 200032, China. · Department of Interventional Radiology, Zhongshan Hospital Fudan University, Shanghai 200032, China. · Department of Radiology, Zhongshan Hospital Fudan University, Shanghai 200032, China. · Endoscopy Center, Zhongshan Hospital Fudan University, Shanghai 200032, China. · Department of Traditional Chinese Medicine, Zhongshan Hospital Fudan University, Shanghai 200032, China. · Department of Liver Surgery, Zhongshan Hospital Fudan University, Shanghai 200032, China. · Department of Medical Oncology, Zhongshan Hospital Fudan University, Shanghai 200032, China. ·Zhonghua Wai Ke Za Zhi · Pubmed #31826595.

ABSTRACT:

2 Article Cancer-FOXP3 directly activated CCL5 to recruit FOXP3 2017

Wang, X / Lang, M / Zhao, T / Feng, X / Zheng, C / Huang, C / Hao, J / Dong, J / Luo, L / Li, X / Lan, C / Yu, W / Yu, M / Yang, S / Ren, H. ·Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer; Key Laboratory of Cancer Prevention and Therapy, Department of Pancreatic Cancer, Tianjin, China. · The State Key Laboratory of Experimental Hematology, Institute of Hematology and Hospital of Blood Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, China. · Department of Nutrition and Food Hygiene, School of Public Health, Tianjin Medical University, Tianjin, China. · Department of Gynaecology, Hepingqu Gynaecology and Obsterics Hospital, Tianjin, China. · Penn State College of Medicine, Hershey, PA, USA. ·Oncogene · Pubmed #27991933.

ABSTRACT: Forkheadbox protein 3 (FOXP3), initially identified as a key transcription factor for regulatory T cells (Treg cells), was also expressed in many tumors including pancreatic ductal adenocarcinoma (PDAC). However, its role in PDAC progression remains elusive. In this study, we utilized 120 PDAC tissues after radical resection to detect cancer-FOXP3 and Treg cells by immunohistochemistry and evaluated clinical and pathological features of these patients. Cancer-FOXP3 was positively correlated with Treg cells accumulation in tumor tissues derived from PDAC patients. In addition, high cancer-FOXP3 expression was associated with increased tumor volumes and poor prognosis in PDAC especially combined with high levels of Treg cells. Overexpression of cancer-FOXP3 promoted the tumor growth in immunocompetent syngeneic mice but not in immunocompromised or Treg cell-depleted mice. Furthermore, CCL5 was directly trans-activated by cancer-FOXP3 and promoted the recruitment of Treg cells from peripheral blood to the tumor site in vitro and in vivo. This finding has been further reinforced by the evidence that Treg cells recruitment by cancer-FOXP3 was impaired by neutralization of CCL5, thereby inhibiting the growth of PDAC. In conclusion, cancer-FOXP3 serves as a prognostic biomarker and a crucial determinant of immunosuppressive microenvironment via recruiting Treg cells by directly trans-activating CCL5. Therefore, cancer-FOXP3 could be used to select patients with better response to CCL5/CCR5 blockade immunotherapy.

3 Article Increased expression of the lncRNA PVT1 is associated with poor prognosis in pancreatic cancer patients. 2015

Huang, C / Yu, W / Wang, Q / Cui, H / Wang, Y / Zhang, L / Han, F / Huang, T. ·Department of Hepatopancreatobiliary Surgery, The Affiliated Tumor Hospital of Zhengzhou University, Zhengzhou, China - taohuang1973@126.com. ·Minerva Med · Pubmed #25668599.

ABSTRACT: AIM: Long non-coding RNA PVT1 (lncRNA PVT1) has been identified and it plays an oncogenic role in various human cancers. However, its roles in pancreatic cancer remain unclear. The aim of this paper was to explore the PVT1 expression levels and relationship with survival of patients with pancreatic ductal adenocarcinoma (PDAC) and to establish the significance of PVT1 in the development and progression of PDAC. METHODS: In this study, quantitative real-time polymerase chain reaction was performed to analyze the expression levels of lncRNA PVT1 in paired PDAC and adjacent nontumor tissues. The association of PVT1 expression with clinicopathological features was analyzed. Kaplan-Meier survival analysis was performed to analyze the association of PVT1 expression with overall survival rate of patients with PDAC. Univariate and multivariate Cox regression analyses were carried out to analyze the prognostic significance of PVT1 expression. RESULTS: The study results showed that the PVT1 expression was significantly increased in PDAC tissues compared to adjacent nontumor tissues. The expression of PVT1 was associated with clinical stage and N-classification (P<0.05). Patients with high PVT1 expression level had shorter overall survival times compared to those with low PVT1 expression level (P<0.05). Univariate and multivariate Cox regression analyses suggested that PVT1 might be an independent prognostic factor for poor overall survival rate in patients with PDAC. CONCLUSION: The study findings suggested that the increased expression of lncRNA PVT1 in PDAC was correlated with tumor progression, and PVT1 might be a potential molecular biomarker for predicting the prognosis of patients with PDAC.

4 Article β2-AR-HIF-1α: a novel regulatory axis for stress-induced pancreatic tumor growth and angiogenesis. 2013

Shan, T / Ma, J / Ma, Q / Guo, K / Guo, J / Li, X / Li, W / Liu, J / Huang, C / Wang, F / Wu, E. ·Department of Hepatobiliary Surgery, First Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an, Shaanxi, China. ·Curr Mol Med · Pubmed #23745588.

ABSTRACT: The purpose of this study was to test the hypothesis that chronic stress in a negative social and psychological state plays a critical role in pancreatic cancer development and progression. In this study, we created a new stress model system to determine the effects of chronic stress on pancreatic cancer progression. Here, we show that chronic stress not only causes depression in mice, most likely attributed to an elevated level of epinephrine, but also induces pancreatic cancer progression. We provide evidence that the pancreatic cancer progression induced by chronic stress could be blocked to a significant degree by β2-AR inhibitor ICI118 551 or HIF-1α inhibitor 2-methoxyestradiol. Moreover, establishment of pancreatic cancer in mice exposed to chronic stress was accompanied by up-regulation of the expression of MMP-2, MMP-9, and VEGF, mediated by a HIF- 1α-dependent β-AR signaling pathway. Our data suggest that the β2-AR-HIF-1α axis regulates stress-induced pancreatic tumor growth and angiogenesis. This study may have a therapeutic or preventive potential for the patients with pancreatic cancer who are especially prone to psychosocial stress challenges.

5 Article The expression and clinical significance of pSTAT3, VEGF and VEGF-C in pancreatic adenocarcinoma. 2012

Huang, C / Huang, R / Chang, W / Jiang, T / Huang, K / Cao, J / Sun, X / Qiu, Z. ·Department of General Surgery, Shanghai Jiao Tong University, Shanghai, People's Republic of China. ·Neoplasma · Pubmed #22082308.

ABSTRACT: Signal transducers and activators of transcription 3 (STAT3) is a central cytoplasmic transcription factor and regulates a number of pathways important in tumorigenesis including cell cycle progression, apoptosis, tumor angiogenesis, invasion and metastasis.This study aims to investigate the expression of pSTAT3, VEGF and VEGF-C in pancreatic adenocarcinoma and their relations to the clinicopathological features, tumor angiogenesis and prognosis. In the present study, the expression of pSTAT3, VEGF and VEGF-C and microvascular density (MVD) were examined via immunohistochemistry. The clinicopathological information was collected and patients were regularly followed up. The relationship between the parameters and the clinicopathological features were analyzed, and the univariate and multivariate prognostic factors were also analyzed. The expression of pSTAT3 in tumor tissues was significantly higher in contrast to that in normal tissues, and pSTAT3 was related to VEGF and VEGF-C expression, MVD, tumor size, lymphogenous status and TNM staging (P<0.05). Survival analysis suggested that tumor size, TNM staging, pSTAT3 and VEGF expression were risk factors of prognosis, but no independent factors were found. We concluded that pSTAT3, which was a risk factor of prognosis, was abnormally expressed in pancreatic adenocarcinoma and related to tumor size, TNM staging and lymphatic metastasis. pSTAT3 may promote tumor angiogenesis via up-regulating VEGF on protein and even gene levels, and enhance the early lymphatic metastasis through VEGF-C. Better understanding of STAT3 signaling pathways in angiogenesis may contribute to the development of novel therapeutic strategies in angiogenesis and metastasis of pancreatic cancer.

6 Article The effects and mechanisms of blockage of STAT3 signaling pathway on IL-6 inducing EMT in human pancreatic cancer cells in vitro. 2011

Huang, C / Yang, G / Jiang, T / Zhu, G / Li, H / Qiu, Z. ·Department of General Surgery, Affiliated People's Hospital, Shanghai, PR, China. ·Neoplasma · Pubmed #21744993.

ABSTRACT: Aberrant Signal transducers and activators of transcription-3 (STAT3) signaling pathway is a major cause of tumor invasion and metastasis; the underlying mechanisms, however, are not well understood. Epithelial-mesenchymal transition (EMT) is an early event that occurs during invasion of cancers of an epithelial origin. It remains elusive whether STAT3signaling pathway is involved in EMT. The objective of this study was to evaluate the effect of blockage of STAT3 signaling pathway on IL-6 inducing EMT in human pancreatic cancer cells. We used SW1990 cells and induced them to undergo EMT by exposing these cells to soluble factor interleukin-6 (IL-6). The expression of Snail, E-cadherin, and Twist was detected by reverse transcription-PCR, real-time PCR, and Western blotting. Cell morphology was observed under invert phase-contrast microscope.The invasion ability was determined by cell invasion assay in vitro. Our results demonstrated that STAT3 signaling pathway was involved in pancreatic cancer cell invasion and EMT, and that EMT induced by IL-6 was associated with the activation of STAT3 signaling pathway. Inhibition of STAT3 signaling pathway by silencing of the STAT3 gene with RNAi blocked STAT3 signaling pathway activation and suppressed EMT in pancreatic cancer cells. Collectively, the STAT3 signaling pathway plays an important role in the process of EMT of pancreatic cancer by regulating Snail gene expression. Better understanding of STAT3 signaling pathways in EMT may contribute to development of novel therapeutic strategies in invasion and metastasis of pancreatic cancer.