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Pancreatic Neoplasms: HELP
Articles by W. Zhang
Based on 5 articles published since 2010
(Why 5 articles?)
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Between 2010 and 2020, W. Zhang wrote the following 5 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Clinical Trial A randomized phase II of gemcitabine and sorafenib versus sorafenib alone in patients with metastatic pancreatic cancer. 2012

El-Khoueiry, A B / Ramanathan, R K / Yang, D Y / Zhang, W / Shibata, S / Wright, J J / Gandara, D / Lenz, H J. ·Division of Medical Oncology, Keck School of Medicine, Norris Comprehensive Cancer Center, University of Southern California, 1441 Eastlake Ave, Suite 3440, Los Angeles, CA 90033, USA. elkhouei@usc.edu ·Invest New Drugs · Pubmed #21424698.

ABSTRACT: PURPOSE: Patients with metastatic pancreatic cancer have limited therapeutic options. The role of the Ras-Raf-MAPK pathway and of vascular endothelial growth factor in pancreatic carcinogenesis provided the rational to evaluate the efficacy of sorafenib with or without gemcitabine in a randomized phase II study. METHODS: Patients with metastatic pancreatic cancer were randomized to sorafenib alone (arm A) or sorafenib with gemcitabine (arm B). RESULTS: Arm A was closed to accrual at interim analysis due to the lack of objective response. Median PFS and OS were 2.3 and 4.3 months respectively. There was one partial response among the 37 patients in arm B. Median PFS and OS were 2.9 and 6.5 months respectively. There were more grade 3 and 4 toxicities in arm B with the most common being neutropenia (17%), thrombocytopenia (8%), alkaline phosphatase elevation (14%), venous thromboembolism (8%), diarrhea, hypokalemia and ALT elevation (5%) each. Several associations were noted between single nucleotide polymorphisms in ribonucleotide reductase, Cox-2, vascular endothelial growth factor and survival in patients treated with gemcitabine and sorafenib. CONCLUSIONS: Neither sorafenib alone or sorafenib in combination with gemcitabine manifested promising activity in metastatic pancreatic cancer.

2 Article [The role of Hong's single-stitch duct to mucosa pancreaticojejunostomy in laparoscopic pancreaticoduodenectomy]. 2017

Hong, D F / Liu, Y H / Zhang, Y H / Wang, Y C / Wang, Z M / Wu, W D / Shen, G L / Zhang, J G / Zhang, W / Cheng, J / Peng, S Y. ·Department of Hepatobiliary and Pancreatic Surgery, Minimally Invasive Surgery, Zhejiang Provincial People's Hospital, Hangzhou 310014, China. ·Zhonghua Wai Ke Za Zhi · Pubmed #28162214.

ABSTRACT:

3 Article Yes-associated protein mediates immune reprogramming in pancreatic ductal adenocarcinoma. 2017

Murakami, S / Shahbazian, D / Surana, R / Zhang, W / Chen, H / Graham, G T / White, S M / Weiner, L M / Yi, C. ·Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC, USA. ·Oncogene · Pubmed #27546622.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is characterized by a high degree of inflammation and profound immune suppression. Here we identify Yes-associated protein (Yap) as a critical regulator of the immunosuppressive microenvironment in both mouse and human PDAC. Within Kras:p53 mutant pancreatic ductal cells, Yap drives the expression and secretion of multiple cytokines/chemokines, which in turn promote the differentiation and accumulation of myeloid-derived suppressor cells (MDSCs) both in vitro and in vivo. Pancreas-specific knockout of Yap or antibody-mediated depletion of MDSCs promoted macrophage reprogramming, reactivation of T cells, apoptosis of Kras mutant neoplastic ductal cells and pancreatic regeneration after acute pancreatitis. In primary human PDAC, YAP expression levels strongly correlate with an MDSC gene signature, and high expression of YAP or MDSC-related genes predicts decreased survival in PDAC patients. These results reveal multifaceted roles of YAP in PDAC pathogenesis and underscore its promise as a therapeutic target for this deadly disease.

4 Article Manganese superoxide dismutase expression is negatively associated with microRNA-301a in human pancreatic ductal adenocarcinoma. 2015

Pandit, H / Zhang, W / Li, Y / Agle, S / Li, X / Li, S P / Cui, G / Li, Y / Martin, R C G. ·Department of Surgery, Division of Surgical Oncology, University of Louisville School of Medicine, Louisville, KY, USA. · Department of Pharmacology and Toxicology, University of Louisville School of Medicine, Louisville, KY, USA. · Department of Hand Surgery, China-Japan Union Hospital, Jilin University, Changchun, Jilin, China. · Department of Cancer Biology, Lerner Research Institute, Cleveland Clinic/NB40, Cleveland, OH, USA. ·Cancer Gene Ther · Pubmed #26384137.

ABSTRACT: Manganese superoxide dismutase (MnSOD) expression has been found to be low in human pancreatic ductal adenocarcinoma (PDAC). Previously, we have reported that microRNA-301a (miR-301a) was found being upregulated via nuclear factor-κB (NF-κB) feedback loop in human PDAC. In this study, we investigate whether the miR-301a expression level is associated with MnSOD expression in human PDAC. We established a xenograft PDAC mouse model using transfected PanC-1 cells (miR-301a antisense or scrambled control) to investigate tumor growth and the interaction between MnSOD and miR-301a. The animal study indicated that miR-301a antisense transfection could significantly decrease the growth rate of inoculated PDAC cells, and this decrease in tumor growth rate is associated with increased MnSOD expression. To evaluate the MnSOD-miR-301a correlation in human PDAC, we have analyzed a total of 60 PDAC specimens, along with 20 normal pancreatic tissue (NPT) specimens. Human specimens confirmed a significant decrease of MnSOD expression in PDAC specimens (0.88±0.38) compared with NPT control (2.45±0.76; P<0.05), whereas there was a significant increase in miR-301a levels in PDAC specimens (0.89±0.28) compared with NPT control (0.25±0.41; P<0.05). We conclude that MnSOD expression is negatively associated with miR-301a levels in PDAC tissues, and lower miR-301a levels are associated with increased MnSOD expression and inhibition of PDAC growth.

5 Article High-resolution melting analysis of PCDH10 methylation levels in gastric, colorectal and pancreatic cancers. 2010

Yu, B / Yang, H / Zhang, C / Wu, Q / Shao, Y / Zhang, J / Guan, M / Wan, J / Zhang, W. ·Biomedical Research Institute, Shenzhen-PKU-HKUST Medical Center, China. ·Neoplasma · Pubmed #20353276.

ABSTRACT: Protocadherins are celladhesion molecules with 6 or 7 cadherin motifs in their extracellular domain and various cyotoplasmic domains. PCDH10 was characterized a novel tumor suppressive gene in and was epigenetically silenced in multiple haematologic malignancies as well as some solid tumors such as gastric cancer, nasopharyngeal carcinoma and esophageal carcinoma. High-resolution melting (HRM) analysis has been used as a novel tool for analysis of promoter methylation. In our study, we used HRM analysis to detect the methylation levels of PCDH10 gene in 100 gastric cancers, 100 colorectal cancers, 70 pancreatic cancers and equal number of adjacent normal tissues. The frequency of PCDH10 methylation in all three types of cancers was significantly higher than that in normal tissues. Consistent with previous reports, expression levels of PCDH10 were inversely correlated with methylation levels. But we didn't find significant association between PCDH10 methylation status and TNM staging in all three types of cancers. In summary, application of HRM analysis to large amount of clinical samples proves to be a fast and high-throughput way to investigate the epigenetic status of PCDH10. And this is the first study to evaluate the prevalence of PCDH10 methylation based on large amount of tumor samples, showing that epigenetic regulation of PCDH10 was associated with carcinogenesis.