Pick Topic
Review Topic
List Experts
Examine Expert
Save Expert
  Site Guide ··   
Pancreatic Neoplasms: HELP
Articles by L. Wang
Based on 12 articles published since 2010
(Why 12 articles?)
||||

Between 2010 and 2020, L. Wang wrote the following 12 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Review Positron emission tomography modalities prevent futile radical resection of pancreatic cancer: A meta-analysis. 2017

Wang, L / Dong, P / Wang, W G / Tian, B L. ·Department of Pancreatic Surgery, West China Hospital, Sichuan University, Chengdu 610041, China. · Department of Nuclear Medicine, West China Hospital, Sichuan University, Chengdu 610041, China. · Department of Pancreatic Surgery, West China Hospital, Sichuan University, Chengdu 610041, China. Electronic address: tianbole@163.com. ·Int J Surg · Pubmed #28890410.

ABSTRACT: BACKGROUND: Numerous distant metastases were not detected preoperatively. Positron emission tomography (PET) has been used for oncology diagnosis recently. However, it remains controversial whether PET modality is a more efficient way in detecting unresectable features for radical resection of pancreatic cancer (PC). This meta-analysis aims to validate the efficiency of PET modalities (including PET and PET/CT) in preoperative assessment of PC, and compare them with computed tomography (CT). METHODS: PubMed, EMBASE, Science Citation Index and The Cochrane Library were searched to identify relevant studies. Both PET modality and CT had been performed for all the included patients. A meta-analysis was performed to compare the ability of PET modalities in detecting occult distant metastases and regional lymph nodes invasion with that of CT. RESULTS: 17 clinical studies that recruited 1343 patients were included. This meta-analysis indicated that PET modalities were more efficient in detecting true positive distant metastases compared with CT (OR = 1.52, 95%CI: 1.23-1.88). In subgroup analysis, when compared with CT alone, PET/CT also showed greater utility in detecting distant metastases (OR = 1.66, 95%CI: 1.31-2.08). There was no definite difference in detecting regional lymph nodes invasion between PET modalities and CT (OR = 0.97, 95%CI: 0.63-1.47). CONCLUSION: Compared with CT, PET/CT provides extensive possibility to avoid futile radical resection by detecting occult metastases of PC preoperatively. Surgeons, especially in developing countries, should take PET modalities as a routine preoperative assessment before making operative plan for PC patients.

2 Review Long Non-Coding RNA: An Emerging Paradigm of Pancreatic Cancer. 2016

Han, T / Hu, H / Zhuo, M / Wang, L / Cui, J-J / Jiao, F / Wang, L-W. ·Department of Medical Oncology and Pancreatic Cancer Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine; Shanghai Key Laboratory of Pancreatic Diseases, 650 New Songjiang Road, Shanghai 201620, China. jiao_f@outlook.com. · . yzwlw@hotmail.com. ·Curr Mol Med · Pubmed #27686798.

ABSTRACT: Pancreatic cancer remains a worldwide issue and burden that is hard to resolve given its low resection rate and chemo-resistance. Early diagnosis and early treatment are critical for conquering pancreatic cancer. Therefore, new biomarkers for diagnosis and prognosis are urgently needed. Previously, researchers mainly focused on protein-coding genetic and epigenetic changes in many types of cancers, and regarded the noncoding part as waste. Recently, however, long non-coding RNA (lncRNA) has emerged as a major participant in carcinogenesis, as it regulates cell proliferation, migration, invasion, metastasis, chemo-resistance, etc. The underlying mechanisms are summarized as signaling, decoy, guide and scaffold, yet the specific regulation networks remain to be uncovered. Several studies have revealed that some lncRNAs are dysregulated in pancreatic cancer, participating in biological functions. In this review, we will briefly outline the functional lncRNAs in pancreatic cancer, decipher possible mechanisms of lncRNAs, and further explore their significance in pancreatic cancer.

3 Clinical Trial A phase II study of the HSP90 inhibitor AUY922 in chemotherapy refractory advanced pancreatic cancer. 2016

Renouf, D J / Hedley, D / Krzyzanowska, M K / Schmuck, M / Wang, L / Moore, M J. ·British Columbia Cancer Agency, University of British Columbia, 600 West 10th Avenue, Vancouver, BC, V5Z4E6, Canada. drenouf@bccancer.bc.ca. · University Health Network-Princess Margaret Cancer Centre, Toronto, ON, Canada. · British Columbia Cancer Agency, University of British Columbia, 600 West 10th Avenue, Vancouver, BC, V5Z4E6, Canada. ·Cancer Chemother Pharmacol · Pubmed #27422303.

ABSTRACT: OBJECTIVES: AUY922 is a novel heat shock protein inhibitor with preclinical activity in pancreatic cancer. This phase II study evaluated the efficacy of AUY922 in patients with advanced pancreatic cancer previously treated with chemotherapy. METHODS: In this single-arm, Simon two-stage phase II trial, patients with metastatic or locally advanced pancreatic ductal adenocarcinoma who had progressed on at least one line of chemotherapy and were of good performances status (ECOG 0 or 1) were treated with AUY922 at a dose of 70 mg/m(2) IV weekly. The primary endpoint was disease control rate (objective response and stable disease ≥16 weeks). RESULTS: Twelve patients were accrued, all of whom received treatment. At least possibly related ≥grade 3 adverse events included fatigue (8 %) and AST elevation (8 %). Ten patients were evaluable for response with 1 (10 %) having stable disease and 9 (90 %) progressive disease. The median progression-free survival was 1.6 months, and the median overall survival was 2.9 months. CONCLUSIONS: AUY922 was not associated with significant efficacy in previously treated patients with advanced pancreatic cancer.

4 Clinical Trial A phase II study of erlotinib in gemcitabine refractory advanced pancreatic cancer. 2014

Renouf, D J / Tang, P A / Hedley, D / Chen, E / Kamel-Reid, S / Tsao, M S / Tran-Thanh, D / Gill, S / Dhani, N / Au, H J / Wang, L / Moore, M J. ·British Columbia Cancer Agency, University of British Columbia, Vancouver, BC, Canada. Electronic address: drenouf@bccancer.bc.ca. · Tom Baker Cancer Centre, Calgary, AB, Canada. · University Health Network-Princess Margaret Cancer Centre, Toronto, ON, Canada. · British Columbia Cancer Agency, University of British Columbia, Vancouver, BC, Canada. · Cross Cancer Institute, Edmonton, AB, Canada. ·Eur J Cancer · Pubmed #24857345.

ABSTRACT: BACKGROUND: Erlotinib induced skin toxicity has been associated with clinical benefit in several tumour types. This phase II study evaluated the efficacy of erlotinib, dose escalated to rash, in patients with advanced pancreatic cancer previously treated with gemcitabine. METHODS: Erlotinib was given at an initial dose of 150 mg/day, and the dose was escalated by 50mg every 2 weeks (to a maximum of 300 mg/day) until >grade 1 rash or other dose limiting toxicities occurred. Erlotinib pharmacokinetics were performed, and baseline tumour tissue was collected for mutational analysis and epidermal growth factor receptor (EGFR) expression. The primary end-point was the disease control rate (objective response and stable disease >8 weeks). RESULTS: Fifty-one patients were accrued, and 49 received treatment. Dose-escalation to 200-300 mg of erlotinib was possible in 9/49 (18%) patients. The most common ⩾ grade 3 adverse events included fatigue (6%), rash (4%) and diarrhoea (4%). Thirty-seven patients were evaluable for response, and the best response was stable disease in 12 patients (32% (95% confidence interval (CI) 17-47%)). Disease control was observed in nine patients (24% (95% CI: 10-38%)). Median survival was 3.8 months, and 6 month overall survival rate was 32% (95% CI 19-47%). Mutational analysis and EGFR expression were performed on 29 patients, with 93% having KRAS mutations, none having EGFR mutations, and 86% expressing EGFR. Neither KRAS mutational status nor EGFR expression was associated with survival. CONCLUSIONS: Erlotinib dose escalated to rash was well tolerated but not associated with significant efficacy in non-selected patients with advanced pancreatic cancer.

5 Article [Clinicopathological features and outcome of gastroenteropancreatic high-grade (WHO G3) neuroendocrine tumors: a study of 60 cases]. 2020

Huang, D / Tan, C / Weng, W W / Ni, S J / Wang, L / Sheng, W Q. ·Department of Pathology, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University; Institute of Pathology, Fudan University, Shanghai 200032, China. ·Zhonghua Bing Li Xue Za Zhi · Pubmed #31914528.

ABSTRACT:

6 Article PKR2 and β-catenin genes regulates pancreatic cancer chemosensitivity. 2017

Zhong, R-L / Li, Y / Fang, Z / Fang, K-F / Wang, L. ·Cancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. liwang1456@hotmail.com. ·Eur Rev Med Pharmacol Sci · Pubmed #28121357.

ABSTRACT: OBJECTIVE: Pancreas is a well developed glandular organ lying behind the stomach. Cancer arises in this organ are difficult to identify in the initial stages, even in advanced stages it shows non-specific symptoms, and it is difficult to prognosis. Since they are identified and treated in the last stage, they are less responsive to chemotherapy. Therefore, it is important to study the proteins that are involved in regulating chemosensitivity and chemoresistance. MATERIALS AND METHODS: Initially, using KRAS mutant mice, we developed initial and advanced stage of pancreatic cancer. And we analyzed the expression of PKR2 and β-catenin in different pathological stages of pancreatic cancer using Immunohistology and Western blotting. RESULTS: The histology of the tissue nature confirms and helps to categorize cancer, which shows enlarged nucleus in initial stages and shows clustering of cells in advanced stages. Immunohistological and Western blotting analyzes show prominent increasing in the expression of PKR2 and β-catenin as the tumor develops to the next stages. On the course of initial treatment with cisplatin we find out that PKR2 and β-catenin regulate the chemosensitivity with under-expression when compared with respective controls. In the advanced stages of pancreatic cancer with cisplatin treatment, we observed chemoresistance behavior with overexpression, especially for β-catenin. CONCLUSIONS: The results conclude that using PKR2 and β-catenin we are able to assess the chemosensitivity and chemoresistance nature of pancreatic cancer.

7 Article HGF/Met and FOXM1 form a positive feedback loop and render pancreatic cancer cells resistance to Met inhibition and aggressive phenotypes. 2016

Cui, J / Xia, T / Xie, D / Gao, Y / Jia, Z / Wei, D / Wang, L / Huang, S / Quan, M / Xie, K. ·Department of Gastroenterology, Hepatology and Nutrition, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. · Department of Gastroenterology, Shanghai Changhai Hospital, Second Military Medical University, Shanghai, People's Republic of China. · Department of Oncology, Shanghai Tongji University Affiliated East Hospital, Shanghai, People's Republic of China. · Department of Neurosurgery, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. ·Oncogene · Pubmed #26876216.

ABSTRACT: Hepatocyte growth factor (HGF)/Met signaling has critical roles in pancreatic ductal adenocarcinoma (PDA) development and progression and is considered a potential therapeutic target for this disease. However, the mechanism of aberrant activation of HGF/Met signaling and resistance to Met inhibition in PDA remains unclear. The mechanistic role of cross talk between Forkhead box M1 (FOXM1) and HGF/Met signaling in promotion of PDA growth and resistance to Met inhibition was examined using cell culture, molecular biology and mouse models; and the relevance of our experimental and mechanistic findings were validated using human PDA tissues. Met was markedly overexpressed in both PDA cell lines and pancreatic tumor specimens, and the expression of Met correlated directly with that of FOXM1 in human tumor specimens. Mechanistically, FOXM1 bound to the promoter region of the Met gene and transcriptionally increased the expression of Met. Increased expression of FOXM1 enhanced the activation of HGF/Met signaling and its downstream pathways, including retrovirus-associated DNA sequences/extracellular signal-regulated kinase 1/2, phosphoinositide 3-kinase/AKT and signal transducer and activator of transcription 3. Furthermore, activation of HGF/Met signaling increased the expression and transcriptional activity of FOXM1, and the cross talk between FOXM1 and HGF/Met signaling promoted PDA growth and resistance to Met inhibition. Collectively, our findings identified a positive feedback loop formed by FOXM1 and HGF/Met and revealed that this loop is a potentially effective therapeutic target for PDA.

8 Article Epidemiology, diagnosis, surgical treatment and prognosis of the pancreatic neuroendocrine tumors: Report of 125 patients from one single center. 2015

Yang, M / Tian, B / Zhang, Y / Su, A / Yue, P / Xu, S / Wang, L. ·Department of Hepato-Bilio-Pancreatic Surgery, West China Hospital of Sichuan University, Chengdu, Sichuan Province, The People's Republic of China. ·Indian J Cancer · Pubmed #26905133.

ABSTRACT: OBJECTIVE: The objective of the following study is to summarize the epidemiology of pancreatic neuroendocrine tumors (p-NETs) in our single institution, analyze the diagnostic characteristics, share the experience of surgical treatments and discuss the prognostic factors. METHODS: A retrospective collection and analysis of clinical data of 125 patients with p-NETs which were pathologically confirmed in our hospital from January 2002 to December 2012. RESULTS: A total of 125 patients of which 52 were males and 73 were females. Totally 92 patients had functional p-NETs, while non-functional p-NETs were diagnosed in 33 patients. The most common operative procedures performed were local resection of pancreatic tumor (47.2%), followed by distal pancreatectomy (29.6%). Thirty patients (28%) had post-operative complications, the most common of which was pancreatic fistula (22.4%). The overall survival rate at 5 years was 68.4%. The 5-year survival rate for patients with functional tumors was 75.1%, compared with 50.0% for those with non-functional tumors (P = 0.021). The survival time of patients with R0 resection was statistically longer than that of patients with Not R0 resection (P < 0.005). In univariate analysis, the most powerful predictors of poor outcome were gender, age, tumor size, functional status, surgical margins, lymph node invasion and distant metastasis. However only surgical margin and distant metastasis were significant predictors in multivariate analysis (P = 0.001, 0.047, respectively). CONCLUSION: p-NETs are an uncommon and heterogeneous group of tumors, with a rising incidence. Surgery is the most effective treatment. Surgical margin and distant metastasis were the most significant prognostic factors. Radical resection should be taken more into considerations.

9 Article Effects of gemcitabine on radiosensitization, apoptosis, and Bcl-2 and Bax protein expression in human pancreatic cancer xenografts in nude mice. 2015

Shen, Z T / Wu, X H / Wang, L / Li, B / Zhu, X X. ·Department of Radiation Oncology, Jinling Hospital, Medical School of Nanjing University, Nanjing, China. · Department of Radiation Oncology, Jinling Hospital, Medical School of Nanjing University, Nanjing, China xixuzhucn@163.com. ·Genet Mol Res · Pubmed #26634526.

ABSTRACT: The aim of this study was to evaluate the radiosensitizing effects of gemcitabine towards human pancreatic cancer xenografts. A human pancreatic cancer xenograft model was established in nude mice, 36 of which were randomly divided into 6 treatment groups. Tumors were measured every 2 days, and the tumor volumes, growth delays, and inhibition rates were compared to evaluate the gemcitabine enhancement factor. The apoptotic index was determined by terminal deoxynucleotidyl transferase dUTP nick end-labeling assay, and apoptosis inhibitory protein Bcl-2 and apoptosis-related protein Bax expression were detected by immunohistochemistry. Compared with the control group, xenograft growth was significantly inhibited in the 25 (G25) and 50 mg/kg gemcitabine (G50) groups (P < 0.05). In the 25 (G25R) and 50 (G50R) mg/kg gemcitabine + radiotherapy groups, local tumor growth was significantly inhibited, with inhibition rates of 88.22 and 91.23%, respectively, significantly higher than those of the simple radiotherapy (SR), G25, and G50 groups (44.11, 72.88, and 77.53%, respectively; P < 0.05). The tumor growth delay in the G25R and G50R groups were 9 and 15 days, respectively, higher than the SR, G25, and G50 groups (each 4 days, P < 0.05). The apoptosis of tumor cells in the intervention groups significantly increased, and the apoptotic index among the intervention groups exhibited significant differences (P < 0.05). The immunohistochemical results indicated that Bcl-2 was downregulated to different degrees in the intervention groups, whereas Bax was upregulated (P < 0.05). Therefore, gemcitabine appears to enhance the radiotherapeutic sensitivity of human pancreatic cancer xenografts significantly.

10 Article FoxQ1 is a Novel Molecular Target for Pancreatic Cancer and is Associated with Poor Prognosis. 2015

Zhan, H-X / Xu, J-W / Wang, L / Wu, D / Zhang, G-Y / Hu, S-Y. ·Department of General Surgery, Qilu Hospital, Shandong University, Jinan, Shandong Province, 250012, China. husanyuan1962@hotmail.com. ·Curr Mol Med · Pubmed #26122655.

ABSTRACT: FOXQ1 is an oncogene for a variety of tumors and encodes the forkhead boxrelated transcription factor FoxQ1. However, little is known about the role of FoxQ1 in pancreatic cancer (PC). In this study, we examined FoxQ1 expression in PC cell lines and human PC tissues by quantitative PCR and tissue microarray based immunohistochemical staining (IHC), and investigated the clinical correlation between FoxQ1 tissue levels and the clinicopathological characteristics of PC patients. We found that FoxQ1 mRNA expression was up-regulated both in PC cell lines and tumor tissues. IHC results revealed that FoxQ1 was mainly expressed in the cytoplasm, and to a lesser extent in the nucleus of PC cells. FoxQ1 protein levels were significantly higher in PC tissues when compared with matched non-cancerous tissues, and associated positively with the degree of tumor differentiation. Univariate and multivariate survival analysis revealed that patients with high FoxQ1 expression and advanced TNM stage had poor prognosis (HR=1.856, 95%CI 1.065- 3.234, P=0.029; HR=2.091, 95%CI 1.181-3.705, P=0.01). These data indicate that FoxQ1 expression is negatively associated with the overall survival of PC patients, and that this protein may therefore represent a novel molecular target and new prognostic biomarker for PC.

11 Article Expression and clinical significance of IMP3 in microdissected premalignant and malignant pancreatic lesions. 2015

Wang, B-J / Wang, L / Yang, S-Y / Liu, Z-J. ·Department of Laboratory Medicine, The Second Affiliated Hospital, Nanjing Medical University, Nanjing, 210011, People's Republic of China. ·Clin Transl Oncol · Pubmed #25183049.

ABSTRACT: INTRODUCTION: Insulin-like growth factor 2 (IGF-2) mRNA-binding protein 3 (IMP3) is overexpressed in pancreatic cancer, while remaining undetectable in the normal pancreas, indicating its important role in pancreatic cancer pathogenesis. The role of IMP3 in pancreatic carcinogenesis has not been fully understood. The main goal of this study was to probe the expression profile of IMP3 in different stages of pancreatic ductal adenocarcinoma (PDAC) development, and evaluate their prognostic significance in PDAC patients. MATERIALS AND METHODS: We used quantitative real-time RT-PCR combined manual microdissection to precisely detect IMP3 expression in 97 microdissected foci from 50 patients with PDAC. Nonparametric test, Log-rank test and Cox regression analysis were used to evaluate the clinical significance of DNMTs expression. RESULTS: Expression of IMP3 increased from normal duct to pancreatic intraductal neoplasia and to PDAC. IMP3 mRNA expression statistically correlated with TNM staging. Univariate analysis showed that high level of IMP3 expression, tumor differentiation, TNM staging and alcohol consumption were statistically significant risk factors. Multivariate analysis showed that high level of IMP3 expression and tumor differentiation were statistically significant independent poor prognostic factors. CONCLUSIONS: These results suggested that pancreatic carcinogenesis involves an increased IMP3 mRNA expression, and it may become valuable diagnostic and prognostic markers as well as potential therapeutic targets for pancreatic cancer.

12 Article Activation of glucagon-like peptide-1 receptor inhibits tumourigenicity and metastasis of human pancreatic cancer cells via PI3K/Akt pathway. 2014

Zhao, H / Wang, L / Wei, R / Xiu, D / Tao, M / Ke, J / Liu, Y / Yang, J / Hong, T. ·Department of Endocrinology and Metabolism, Peking University Third Hospital, Beijing, China. ·Diabetes Obes Metab · Pubmed #24641303.

ABSTRACT: AIMS: It has been reported that glucagon-like peptide-1 (GLP-1) agents are associated with an increased risk of pancreatic cancer in patients with type 2 diabetes. Reports have indicated that GLP-1 promotes pancreatic metaplasia and premalignant lesions. The aims of this study were to determine the effects of GLP-1-based therapy on pancreatic cancer cells. METHODS: Immunohistochemistry was used to investigate GLP-1 receptor (GLP-1R) expression in 30 human pancreatic cancer tissues. We also analysed associated clinicopathological data and each patient's prognosis. Two human pancreatic cancer cell lines were used to evaluate the in vitro effects of the GLP-1R agonist liraglutide on cell growth, migration and invasion. Mouse xenograft models of human pancreatic cancer were established to evaluate the effects of liraglutide in vivo. RESULTS: Human pancreatic cancer tissues showed lower levels or a lack of GLP-1R expression when compared with levels in the tumour-adjacent pancreatic tissues. Negative GLP-1R expression occurred more frequently in advanced tumours with larger diameters and lymphatic metastasis, and was associated with a poor prognosis. GLP-1R activation with liraglutide inhibited tumourigenicity and metastasis of human pancreatic cancer cells in vitro and in vivo. Akt activation was dose-dependently inhibited by liraglutide, and the PI3K inhibitors, LY294002 and wortmannin, displayed similar suppressive effects to liraglutide in human pancreatic cancer cells. CONCLUSIONS: GLP-1R activation has an antitumour effect on human pancreatic cancers via inhibition of the PI3K/Akt pathway. This finding suggests that GLP-1-based therapies may be beneficial, rather than harmful, in treating type 2 diabetic patients with pancreatic cancer.