Pick Topic
Review Topic
List Experts
Examine Expert
Save Expert
  Site Guide ··   
Pancreatic Neoplasms: HELP
Articles by Lei Dong
Based on 5 articles published since 2009
(Why 5 articles?)
||||

Between 2009 and 2019, Lei Dong wrote the following 5 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Editorial Pancreatic cancer: translational research aspects and clinical implications. 2012

Ansari, Daniel / Chen, Bi-Cheng / Dong, Lei / Zhou, Meng-Tao / Andersson, Roland. · ·World J Gastroenterol · Pubmed #22509073.

ABSTRACT: Despite improvements in surgical techniques and adjuvant chemotherapy, the overall mortality rates in pancreatic cancer have generally remained relatively unchanged and the 5-year survival rate is actually below 2%. This paper will address the importance of achieving an early diagnosis and identifying markers for prognosis and response to therapy such as genes, proteins, microRNAs or epigenetic modifications. However, there are still major hurdles when translating investigational biomarkers into routine clinical practice. Furthermore, novel ways of secondary screening in high-risk individuals, such as artificial neural networks and modern imaging, will be discussed. Drug resistance is ubiquitous in pancreatic cancer. Several mechanisms of drug resistance have already been revealed, including human equilibrative nucleoside transporter-1 status, multidrug resistance proteins, aberrant signaling pathways, microRNAs, stromal influence, epithelial-mesenchymal transition-type cells and recently the presence of cancer stem cells/cancer-initiating cells. These factors must be considered when developing more customized types of intervention ("personalized medicine"). In the future, multifunctional nanoparticles that combine a specific targeting agent, an imaging probe, a cell-penetrating agent, a biocompatible polymer and an anti-cancer drug may become valuable for the management of patients with pancreatic cancer.

2 Article The impact of unplanned conversion to an open procedure during minimally invasive pancreatectomy. 2018

Stiles, Zachary E / Dickson, Paxton V / Deneve, Jeremiah L / Glazer, Evan S / Dong, Lei / Wan, Jim Y / Behrman, Stephen W. ·Division of Surgical Oncology, Department of Surgery, University of Tennessee Health Science Center, Memphis, Tennessee. · Division of Biostatistics, Department of Preventive Medicine, University of Tennessee Health Science Center, Memphis, Tennessee. · Division of Surgical Oncology, Department of Surgery, University of Tennessee Health Science Center, Memphis, Tennessee. Electronic address: sbehrman@uthsc.edu. ·J Surg Res · Pubmed #29804849.

ABSTRACT: BACKGROUND: Minimally invasive pancreatic resection (MIPR) is being increasingly utilized. Outcomes for patients experiencing unplanned conversion to an open procedure during MIPR have been incompletely assessed. We sought to determine the short-term outcomes and factors associated with unplanned conversion during MIPR. METHODS: A retrospective cohort study using the American College of Surgeons National Surgical Quality Improvement Program pancreatectomy-targeted data set was conducted. Successful MIPR was compared with unplanned conversion. Propensity matching was used to separately compare unplanned conversion during MIPR with planned open pancreatectomy. RESULTS: Unplanned conversion occurred in 24.6% of 350 attempted minimally invasive pancreatoduodenectomy (MIPD) and 19.6% of 1174 attempted minimally invasive distal pancreatectomy (MIDP). Conversion was associated with greater overall morbidity and 30-day mortality compared with successful MIPR for both MIPD and MIDP. After matching, unplanned conversion resulted in outcomes equivalent or inferior to open pancreatectomy. Factors significantly associated with unplanned conversion during MIPD included intermediate gland texture, vascular resection, hypertension, disseminated cancer, and chronic steroid use. For MIDP, male sex, hard gland texture, vascular resection, smoking, and recent weight loss were independently associated with conversion. A robotic approach was inversely associated with conversion for MIPD and MIDP. CONCLUSIONS: Unplanned conversion during MIPR is associated with greater morbidity and 30-day mortality. Conversion resulted in outcomes that, at best, mimicked those of open pancreatectomy. Several risk factors including the need for vascular resection are associated with unplanned conversion and should be acknowledged when planning an operative approach.

3 Article Celecoxib suppresses fibroblast growth factor-2 expression in pancreatic ductal adenocarcinoma PANC-1 cells. 2016

Li, Jing / Luo, Miaosha / Wang, Yan / Shang, Boxin / Dong, Lei. ·Department of Gastroenterology, The Second Affiliated Hospital of Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi 710004, P.R. China. · The First Affiliated Hospital of Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi 710000, P.R. China. ·Oncol Rep · Pubmed #27430377.

ABSTRACT: The inhibition of cyclooxygenase (COX)-2 has been reported to suppress growth and induce apoptosis in human pancreatic cancer cells. Nevertheless, the precise biological mechanism of how celecoxib, a selective COX-2 inhibitor, regulates the growth and invasion of pancreatic tumors is not completely understood. It has been shown that fibroblast growth factor-2 (FGF-2) and its receptor levels correlate with the inhibition of cancer cell proliferation, migration and invasion in pancreatic ductal adenocarcinoma (PDAC). Therefore, the aim of the present study was to examine the hypothesis that the antitumor activity of celecoxib in PDAC may be exerted through modulation of FGF-2 function. In the present study, we evaluated the effects of celecoxib on the proliferation, migration, invasion and apoptosis of the PANC-1 cell line. Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR) were used to examine the expression of FGF-2, FGFR-2, ERK1/2 and MMPs. In the present study, FGF-2 and FGFR-2 were expressed in PANC-1 cells and FGF-2 exerted a stimulatory effect on phosphorylated extracellular signal regulated kinase (p-ERK) expression. Celecoxib treatment suppressed FGF-2 and FGFR-2 expression and decreased MMP-2, MMP-9 and p-ERK expression in the PANC-1 cells. Furthermore, celecoxib treatment caused the resistance of PANC-1 cells to FGF-2 induced proliferation, migration and invasion ability, as well as the increase in their apoptotic rate. Our data provide evidence that targeting FGF-2 with celecoxib may be used as an effective treatment in PDAC.

4 Article Peptide tyrosine-tyrosine combined with its receptors exhibits an anti-cancer potential in pancreatic cancer MiaPaCa-2 cell. 2014

Li, Hongxia / Wang, Zhixin / Dong, Lei / Jiang, Jiong / Xu, Xinsen / Zhou, Lei / Wan, Yong. ·Department of Gastroenterology, the First Affiliated Hospital of Xi'an Jiaotong University College of Medicine, Xi'an, Shaanxi 710061, China. Email: diandianliu001@126.com. · Department of Hepatobiliary Surgery, the First Affiliated Hospital of Xi'an Jiaotong University College of Medicine, Xi'an, Shaanxi 710061, China. · Department of Gastroenterology, the First Affiliated Hospital of Xi'an Jiaotong University College of Medicine, Xi'an, Shaanxi 710061, China. ·Chin Med J (Engl) · Pubmed #25533827.

ABSTRACT: BACKGROUND: Pancreatic cancer is a common malignant tumor of the digestive system. It is the fourth major cause of tumor-related death and its morbidity is increasing, and hence it is imperative to develop effective forms of therapy for pancreatic cancer. Peptide tyrosine-tyrosine (PYY) is an important gastrointestinal peptide hormone. According to previous literatures, PYY has been shown to inhibit tumor proliferation in cellular and animal models, but there has been limited research on the detailed mechanism of PYY in pancreatic cancer. This study was to observe the effects of PYY on pancreatic cancer cell and investigate the possible mechanism. METHODS: The expression of Y1, Y2, and Y5 receptors on pancreatic cancer cell lines were detected by reverse transcription quantitative polymerase chain reaction (RT-qPCR). The cytotoxicity of PYY toward the MiaPaCa-2 cell was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay; the cell morphology and structure changes were observed under inverted microscope and transmission electron microscope respectively. Apoptosis and cell cycle were evaluated by flow cytometry. The activity of caspase-3 was determined by activity assay kits and Western blotting. The expression of survivin, vascular endothelial growth factor (VEGF), and cyclooxygenase-2 (COX-2) were determined by RT-qPCR and Western blotting. RESULTS: Expression of Y2 receptor is the most abundant PYY receptor on pancreatic cancer cell. PYY inhibited MiaPaCa-2 cell proliferation, blocked it in G0/G1 phase, increased the proportion of apoptosis cells and caspase-3 activity, and reduced the expression of survivin, VEGF, and COX-2. CONCLUSIONS: PYY weakened the ability of the pancreatic MiaPaCa-2 cell viability through cell cycle blocking and apoptosis inducing. The inhibition effect of PYY may be mediated by the Y2 receptor. The increased caspase-3 activity and reduced expression of survivin, VEGF, and COX-2 may serve as a novel mechanism in PYY inhibition effect on MiaPaCa-2 cell.

5 Article [Thyroid hormone inhibits the growth of pancreatic cancer xenograft in nude mice]. 2013

Wang, Nan / Shang, Boxin / Shi, Haitao / Ma, Hanwei / Jiang, Jiong / Qin, Bin / Dong, Lei. ·Department of Gastroenterology Diseases, Second Affiliated Hospital of Xi'an Jiaotong University College of Medicine, Xi'an 710004, China. E-mail: pumpkingua@126.com. ·Nan Fang Yi Ke Da Xue Xue Bao · Pubmed #23996757.

ABSTRACT: OBJECTIVE: To investigate the therapeutic effect of thyroid hormone in nude mice bearing human pancreatic cancer xenograft. METHODS: A BALB/c nude mouse model bearing pancreatic cancer was established with human pancreatic cancer cell line Bx-PC3. The mouse models were divided randomly into 5 groups, namely the control group treated with distilled water, high and low concentrations of thyroid hormone (T3) groups, and high and low concentration of propylthiouracil (PTU) groups. After intervention for 21 days, the changes in body weight and xenograft tumor volume and weight were measured, and the serum T3 concentration was detected by ELISA assay. The expression of proliferating cell nuclear antigen (PCNA) and microvessel density (MVD) were detected using immunohistochemistry. RESULTS: The body weight of nude mice in T3 groups was significantly reduced after intervention, while that in PTU groups showed no obvious changes. Compared with PTU groups and control group, T3 groups showed significantly reduced tumor volume and weight (P<0.05) with also reduced PCNA expression and MVD, but these effect did not exhibit a dose dependence (P>0.05). CONCLUSION: Thyroid hormone can inhibit the growth of human pancreatic cancer in nude mice by suppressing the proliferation and angiogenesis of the tumor cells, suggesting the potential value of thyroid hormone in pancreatic cancer therapy.