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Pancreatic Neoplasms: HELP
Articles by Y. Wang
Based on 7 articles published since 2010
(Why 7 articles?)

Between 2010 and 2020, Y. Wang wrote the following 7 articles about Pancreatic Neoplasms.
+ Citations + Abstracts
1 Clinical Trial Clinical assessment of palliative radiotherapy for pancreatic cancer. 2018

Tian, Q / Zhang, F / Wang, Y. ·Department of Radiotherapy, The General Hospital of Jinan Military Command, Jinan, Shandong Province, PR China. · Department of Gastroenterology, Shandong Provincial Hospital affiliated to Shandong University, Jinan, Shandong Province, PR China. · Department of Radiotherapy, The General Hospital of Jinan Military Command, Jinan, Shandong Province, PR China. Electronic address: ymwang64@163.com. ·Cancer Radiother · Pubmed #30401617.

ABSTRACT: PURPOSE: To evaluate the feasibility and response to radiotherapy for improving the symptoms and quality of life in patients with pancreatic cancer. PATIENTS AND METHODS: We enrolled 31 eligible patients (20 men, 11 women) with pancreatic cancer who were receiving radiotherapy from February 2012 to February 2014. The prescribed dose was 40 to 42Gy delivered to the planning target volume in seven to ten fractions of 4 to 6Gy. Patients completed Brief Pain Inventory (BPI), Functional Assessment Of Cancer Therapy-Hepatobiliary (FACT-Hep), and European Organisation for Research and Treatment of Cancer Quality Of Life Questionnaire C30 (EORTC QLQ-C30) one week prior to radiotherapy, and one and three months after treatment. The main outcome was the evaluation of the proportion of patients with less pain and reduced clinical symptoms after one month of radiotherapy compared to before treatment according to the BPI, FACT-Hep and EORTC QLQ-C30 scales. RESULTS: Of 31 patients, 28 completed the questionnaires. According to BPI evaluation, symptoms were improved in 57% of patients; the FACT-General (FACT-G) and liver function subscales revealed that there was symptom improvement in 89% and 7.1% of patients, respectively. Six items in the EORTC QLQ-C30 were improved. CONCLUSIONS: Following treatment, pain and clinical symptoms were improved in a considerable proportion of patients with pancreatic cancer, proving that palliative radiotherapy is feasible for pancreatic cancer.

2 Clinical Trial Phase I study of safety and pharmacokinetics of the anti-MUC16 antibody-drug conjugate DMUC5754A in patients with platinum-resistant ovarian cancer or unresectable pancreatic cancer. 2016

Liu, J F / Moore, K N / Birrer, M J / Berlin, S / Matulonis, U A / Infante, J R / Wolpin, B / Poon, K A / Firestein, R / Xu, J / Kahn, R / Wang, Y / Wood, K / Darbonne, W C / Lackner, M R / Kelley, S K / Lu, X / Choi, Y J / Maslyar, D / Humke, E W / Burris, H A. ·Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston joyce_liu@dfci.harvard.edu. · Division of Gynecologic Oncology, Stephenson Oklahoma Cancer Center at the University of Oklahoma Health Sciences Center, Oklahoma City. · Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston. · Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston. · Department of Oncology, New England Cancer Care Specialists, Kennebunk. · Sarah Cannon Research Institute/Tennessee Oncology, PLLC, Nashville. · Early Development, Genentech, South San Francisco, USA. ·Ann Oncol · Pubmed #27793850.

ABSTRACT: BACKGROUND: MUC16 is a tumor-specific antigen overexpressed in ovarian (OC) and pancreatic (PC) cancers. The antibody-drug conjugate (ADC), DMUC5754A, contains the humanized anti-MUC16 monoclonal antibody conjugated to the microtubule-disrupting agent, monomethyl auristatin E (MMAE). PATIENTS AND METHODS: This phase I study evaluated safety, pharmacokinetics (PK), and pharmacodynamics of DMUC5754A given every 3 weeks (Q3W, 0.3-3.2 mg/kg) or weekly (Q1W, 0.8-1.6 mg/kg) to patients with advanced recurrent platinum-resistant OC or unresectable PC. Biomarker studies were also undertaken. RESULTS: Patients (66 OC, 11 PC) were treated with DMUC5754A (54 Q3W, 23 Q1W). Common related adverse events (AEs) in >20% of patients (all grades) over all dose levels were fatigue, peripheral neuropathy, nausea, decreased appetite, vomiting, diarrhea, alopecia, and pyrexia in Q3W patents, and nausea, vomiting, anemia, fatigue, neutropenia, alopecia, decreased appetite, diarrhea, and hypomagnesemia in Q1W patients. Grade ≥3-related AE in ≥5% of patients included neutropenia (9%) and fatigue (7%) in Q3W patients, and neutropenia (17%), diarrhea (9%), and hyponatremia (9%) in Q1W patients. Plasma antibody-conjugated MMAE (acMMAE) and serum total antibody exhibited non-linear PK across tested doses. Minimal accumulation of acMMAE, total antibody, or unconjugated MMAE was observed. Confirmed responses (1 CR, 6 PRs) occurred in OC patients whose tumors were MUC16-positive by IHC (2+ or 3+). Two OC patients had unconfirmed PRs; six OC patients had stable disease lasting >6 months. For CA125, a cut-off of ≥70% reduction was more suitable for monitoring treatment response due to the binding and clearance of serum CA125 by MUC16 ADC. We identified circulating HE4 as a potential novel surrogate biomarker for monitoring treatment response of MUC16 ADC and other anti-MUC16 therapies in OC. CONCLUSIONS: DMUC5754A has an acceptable safety profile and evidence of anti-tumor activity in patients with MUC16-expressing tumors. Objective responses were only observed in MUC16-high patients, although prospective validation is required. CLINICAL TRIAL NUMBER: NCT01335958.

3 Article [Metastatic pancreatic neuroendocrine tumor with ectopic adrenocorticotropic hormone syndrome: a case report]. 2019

Feng, L / Gao, Q / Qi, H Q / Liu, G H / Zhou, W L / Zhai, Z J / Wang, Y. ·Department of Endocrinology, the Fourth Hospital of Hebei Medical University, Shijiazhuang 050035, China. ·Zhonghua Zhong Liu Za Zhi · Pubmed #31550867.

ABSTRACT: -- No abstract --

4 Article [Anatomic study and clinical practice of mesopancreas and total mesopancreatic excision]. 2017

Xu, J Y / Chen, Y R / Liu, C / Tian, L / Wang, J W / Cui, D / Wang, Y / Zhang, W G / Yang, Y M. ·Department of General Surgery, Peking University First Hospital, Beijing 100034, China. ·Zhonghua Wai Ke Za Zhi · Pubmed #28655083.


5 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.

6 Article Genomic sequencing of key genes in mouse pancreatic cancer cells. 2012

Wang, Y / Zhang, Y / Yang, J / Ni, X / Liu, S / Li, Z / Hodges, S E / Fisher, W E / Brunicardi, F C / Gibbs, R A / Gingras, M-C / Li, M. ·Department of Gastroenterology, Changhai Hospital, Second Military Medical University, Shanghai, China. ·Curr Mol Med · Pubmed #22208613.

ABSTRACT: Pancreatic cancer is a multiple genetic disorder with many mutations identified during the progression. Two mouse pancreatic cancer cell lines were established which showed different phenotype in vivo: a non-metastatic cell line, Panc02, and a highly metastatic cell line, Panc02-H7, a derivative of Panc02. In order to investigate whether the genetic mutations of key genes in pancreatic cancer such as KRAS, TP53 (p53), CDKN2A (p16), SMAD4, ZIP4, and PDX-1 contribute to the phenotypic difference of these two mouse pancreatic cancer cells, we sequenced the exonic regions of these key genes in both cell lines and in the normal syngeneic mouse pancreas and compared them with the reference mouse genome sequence. The exons of KRAS, SMAD4, CDKN2A (p16), TP53 (p53), ZIP4, and PDX-1 genes were amplified and the genotype of these genes was determined by Sanger sequencing. The sequences were analyzed with Sequencher software. A mutation in SMAD4 was identified in both cell lines. This homozygote G to T mutation in the first position of codon 174 (GAA) generated a stop codon resulting in the translation of a truncated protein. Further functional analysis indicates that different TGF-β/SMAD signaling pathways were involved in those two mouse cell lines, which may explain the phonotypic difference between the two cells. A single nucleotide polymorphism (SNP) in KRAS gene (TAT to TAC at codon 32) was also identified in the normal pancreas DNA of the syngenic mouse and in both derived tumoral Panc02 and Panc02-H7 cells. No mutation or SNP was found in CDKN2A (p16), TP53 (p53), ZIP4, and PDX-1 genes in these two cell lines. The absence of mutations in genes such as KRAS, TP53, and CDKN2A, which are considered as key genes in the development of human pancreatic cancer suggests that SMAD4 might play a central and decisive role in mouse pancreatic cancer. These results also suggest that other mechanisms are involved in the substantial phenotypic difference between these two mouse pancreatic cancer cell lines. Further studies are warranted to elucidate the molecular pathways that lead to the aggressive metastatic potential of Panc02-H7.

7 Article Suppression effects of AICAR on insulin secretion involved in peroxisome proliferator-activated receptor gamma changes in INS-1 cells. 2010

Guo, H / Zhang, X J / Wang, F / Wang, Y / Shen, Y / Zhao, J J / Gao, L. ·Central Laboratory, Provincial Hospital affiliated to Shandong University, No. 324, Jing 5 Road, Jinan, 250021, China. gaoling1@medmail.com.cn ·J Endocrinol Invest · Pubmed #20101096.

ABSTRACT: BACKGROUND: AMP-activated protein kinase (AMPK) activation is known to attenuate glucose-stimulated insulin secretion (GSIS) in pancreatic beta cells. However, the underlying mechanisms are poorly understood. The purpose of this study was to examine the effects of AMPK activation on insulin secretion and to determine whether peroxisome proliferator-activated receptors (PPAR) are involved in the effects on INS-1 cells. METHODS: INS-1 cells, insulinoma cell lines, were treated with an activator (AICAR) or inhibitor (Compound C) of AMPK as well as inhibitors of PPAR [MK886 and biphenol A diglycidyl ether (BADGE)] for different treatment times. RESULTS: AICAR-induced AMPK activation significantly attenuated GSIS as well as insulin content. Meanwhile, AMPK activation increased the mRNA levels of both PPARalpha and PPARgamma. However, with regard to DNA binding, AMPK activation upregulated PPARgamma only, and it was possible to reduce the increment with the AMPK inhibitor. Moreover, the AICAR-induced suppression of insulin secretion can be counteracted by the PPARgamma inhibitor, BADGE but not the PPARalpha inhibitor. CONCLUSIONS: AICAR-induced glucose-stimulated insulin secretion reduction correlates mainly with PPARgamma changes.