Pick Topic
Review Topic
List Experts
Examine Expert
Save Expert
  Site Guide ··   
Pancreatic Neoplasms: HELP
Articles by Y. Zhu
Based on 4 articles published since 2010
(Why 4 articles?)
||||

Between 2010 and 2020, Y. Zhu wrote the following 4 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Differential MicroRNA Expression Profiles as Potential Biomarkers for Pancreatic Ductal Adenocarcinoma. 2019

Zhu, Y / Wang, J / Wang, F / Yan, Z / Liu, G / Ma, Y / Zhu, W / Li, Y / Xie, L / Bazhin, A V / Guo, X. ·Department of Oncology, International Joint Laboratory for Cell Medical Engineering of Henan Province, Henan University Huaihe Hospital, Kaifeng, Henan, 475000, P. R. China. celltransplant@163.com. · Department of Oncology, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450014, P. R. China. wj68happy@hotmail.com. · Department of Preventive Medicine, Cell Signal Transduction Laboratory, Joint National Laboratory for Antibody Drug Engineering, Institute of Biomedical Informatics, Medical School, Henan University, Kaifeng, Henan, 475004, P. R. China. · Department of Oncology, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450014, P. R. China. · College of Pharmacy and Tianjin Key Laboratory of Molecular Drug Research, Nankai University, Haihe Education Park, Tianjin, 300353, P. R. China. mayonggang@nankai.edu.cn. · Department of Anesthesia, Stanford University, CA 94305, USA. wan.zhu@stanford.edu. · Department of General, Visceral, and Transplantation Surgery, Ludwig-Maximilians-University Munich, Munich, 81377, Germany. alexandr.bazhin@med.uni-muenchen.de. · Department of Preventive Medicine, Cell Signal Transduction Laboratory, Joint National Laboratory for Antibody Drug Engineering, Institute of Biomedical Informatics, Medical School, Henan University, Kaifeng, Henan, 475004, P. R. China. xqguo@henu.edu.cn. ·Biochemistry (Mosc) · Pubmed #31234772.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) remains a clinical challenge due to its poor prognosis. Therefore, the early diagnosis of PDAC is extremely important for achieving a cure. MicroRNAs (miRNAs) could serve as a potential biomarker for the early detection and prognosis of PDAC. In this work we analyzed plasma samples from healthy persons and PDAC patients to assess differential miRNA expression profiles by next generation sequencing technology and bioinformatics analysis. In this way, 165 mature miRNAs were found to be significantly deregulated in the patient group, of which 75 and 90 mature miRNAs were up- and down-regulated compared with healthy individuals, respectively. Furthermore, 1029 novel miRNAs were identified. In conclusion, plasma miRNA expression profiles are different between healthy individuals and patients with PDAC. These data provide a possibility for use of miRNA as diagnostic and prognostic biomarkers of PDAC.

2 Article miR-615-5p is epigenetically inactivated and functions as a tumor suppressor in pancreatic ductal adenocarcinoma. 2015

Gao, W / Gu, Y / Li, Z / Cai, H / Peng, Q / Tu, M / Kondo, Y / Shinjo, K / Zhu, Y / Zhang, J / Sekido, Y / Han, B / Qian, Z / Miao, Y. ·Department of General Surgery, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China. · Department of Hepato-Biliary Surgery, The First People's Hospital of Changzhou, Changzhou, China. · Department of General Surgery, The PLA 105 Hospital, Hefei, China. · Division of Epigenomics, Aichi Cancer Center Research Institute, 1-1 Kanokoden, Nagoya, Japan. · Division of Molecular Oncology, Aichi Cancer Center Research Institute, 1-1 Kanokoden, Nagoya, Japan. · Department of Endocrinology, Nanjing Children's Hospital Affiliated with Nanjing Medical University, Nanjing, China. ·Oncogene · Pubmed #24769899.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is a highly invasive cancer with a poor prognosis. Although microRNA (miRNA) transcripts have a crucial role in carcinogenesis and development, little information is known regarding the aberrant DNA methylation of miRNAs in PDAC. Using methylated DNA immunoprecipitation-chip analysis, we found that miR-615-5p was hypermethylated in its putative promoter region, which silenced its expression in PDAC cell lines. In addition, the overexpression of miR-615-5p in pancreatic cancer cells suppressed cell proliferation, migration and invasion. Insulin-like growth factor 2 (IGF2) is an imprinted gene, and its abnormal expression contributes to tumor growth. Here, we identified IGF2 as a target of miR-615-5p using a luciferase reporter assay. IGF2 upregulation in PDAC tissues was not correlated with a loss of imprinting but was inversely correlated with miR-615-5p downregulation. In addition, miR-615-5p suppressed pancreatic cancer cell proliferation, migration and invasion by directly targeting IGF2, and this effect could be reversed by co-transfection with IGF2. Furthermore, the stable overexpression of miR-615-5p inhibited tumor growth in vivo and was correlated with IGF2 expression. Using RNA sequencing, we further identified miR-615-5p as potentially targeting other genes, such as the proto-oncogene JUNB, and interfering with the insulin signaling pathway. Taken together, our results demonstrate that miR-615-5p was abnormally downregulated in PDAC cells due to promoter hypermethylation, which limited its inhibition of IGF2 and other target genes, thereby contributing to tumor growth, invasion and migration. These data demonstrate a novel and important role of miR-615-5p as a tumor suppressor in PDAC.

3 Article Effectiveness and security of CT-guided percutaneous implantation of (125)I seeds in pancreatic carcinoma. 2014

Yu, Y-P / Yu, Q / Guo, J-M / Jiang, H-T / Di, X-Y / Zhu, Y. ·1 Department of Radiology, Zhejiang Cancer Hospital, Hangzhou, Zhejiang, China. ·Br J Radiol · Pubmed #24734936.

ABSTRACT: OBJECTIVE: To assess the effectiveness and security of CT-guided percutaneous implantation of iodine-125 ((125)I)-labelled seeds in pancreatic carcinoma. METHODS: A total of 36 patients (25 males and 11 females) with an average age of 57 years (range, 39-84 years) were enrolled and categorized into Stage III (27 cases) and Stage IV (9 cases) of pancreatic cancer. There were 3 tumours in the pancreatic head and 33 tumours in the pancreatic body or tail. The average diameter of the tumours was 37.1 mm (range, 15-65 mm). The implantation of (125)I seeds was performed by using 18-G needles (length, 150-200 mm) through the anterior, lateral and posterior approaches. Then, (125)I seeds were loaded and released into the lesions. RESULTS: Implantations were performed via the anterior (23 patients), lateral (9 patients) and posterior (4 patients) approaches. During implantation, 3-14 punctures were performed for each patient, and a total of 164 punctures were recorded. Meanwhile, a total of 657 seeds were implanted with an average of 25.27 (range, 12-50) seeds per patient, and the success rate was 100%. The activity of each seed ranged from 0.55 to 0.65 mCi. A main adverse event occurred in one puncture and minor events in seven punctures. No significant relationship between the punctures or adverse events was identified. No serious complication was detected after the implantations during follow-up visits. CONCLUSION: This study suggested that CT-guided percutaneous implantation of (125)I seeds in a pancreatic carcinoma was relatively safe and effective for treating unresectable pancreatic cancer. ADVANCES IN KNOWLEDGE: The CT-guided percutaneous implantation of (125)I seeds in unresectable pancreatic cancer showed highly successful rates without serious complications.

4 Article (125)I particle implantation combined with chemoradiotherapy to treat advanced pancreatic cancer. 2014

Yu, Y-P / Yu, Q / Guo, J-M / Jiang, H-T / Di, X-Y / Zhu, Y. ·Department of Radiology, Zhejiang Cancer Hospital, Hangzhou, Zhejiang, China. ·Br J Radiol · Pubmed #24625042.

ABSTRACT: OBJECTIVE: To evaluate the therapy effects of (125)I implantation combined with chemoradiotherapy on pancreatic cancer patients. METHODS: 30 patients with Stage III or IV pancreatic cancer were equally divided into two groups (control and treatment group). The patients in the treatment group (nine males, six females) received chemotherapy in the first week and (125)I implantation in the third week, followed by combined chemoradiotherapy in the fifth week. The patients in the control group (10 males, 5 females) received the same treatment except (125)I implantation. The therapy in the control group and treatment group was repeated every 4 weeks. RESULTS: The median conformal radiotherapy dose in the treatment group (30.62 Gy) was significantly lower than that in the control group (47.86 Gy). The total radiation dose was 88.71 ± 27.39 Gy, and the surface activity was 0.6 mCi in the treatment group. After treatment, the average tumour size decreased both in the treatment group [9.17 cm(2), 95% confidence interval (CI): 5.60-12.74, p < 0.001] and in the control group (4.54 cm(2), 95% CI: 2.74-6.35, p < 0.001). The median survival time in the treatment group was 14 months (95% CI: 12.215-14.785) and in the control group was 12 months (95% CI: 10.884-13.116). There was no statistical significance in survival rates between the two groups (χ(2) = 0.908, p = 0.341). CONCLUSION: (125)I implanted into tumour combined with chemoradiotherapy has higher local control rate of advanced pancreatic cancer than chemoradiotherapy. ADVANCES IN KNOWLEDGE: We combined chemoradiotherapy with (125)I implantation to treat advanced pancreatic cancer and obtained a higher local control rate and better quality of life than when using chemoradiatherapy alone.