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Pancreatic Neoplasms: HELP
Articles by Zhuojia Chen
Based on 6 articles published since 2009
(Why 6 articles?)
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Between 2009 and 2019, Zhuo Chen wrote the following 6 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article HBXIP protein overexpression predicts the poor prognosis of pancreatic ductal adenocarcinomas. 2019

Zhou, Xingzhi / Wang, Xuanyu / Duan, Jiahong / Sun, Wenxin / Chen, Zhuo / Li, Qiulan / Ou, Zitong / Jiang, Ge / Ren, Xin / Liu, Shuangping. ·Department of Pathology, Medical College, Dalian University, Dalian 116622, Liaoning, China; Department of Biology, Life Science and Technology College, Dalian University, Dalian 116622, Liaoning, China. · Department of Pathology, Medical College, Dalian University, Dalian 116622, Liaoning, China. · Department of Biology, Life Science and Technology College, Dalian University, Dalian 116622, Liaoning, China. · Department of Pathology, Medical College, Dalian University, Dalian 116622, Liaoning, China. Electronic address: renxin@dlu.edu.cn. · Department of clinical laboratory, Xinhua Hospital Affiliated to Dalian University, Dalian, 116021, China; Department of Pathology, Medical College, Dalian University, Dalian 116622, Liaoning, China. Electronic address: liushuangping@dlu.edu.cn. ·Pathol Res Pract · Pubmed #30583814.

ABSTRACT: BACKGROUND: Hepatitis B virus X-interacting protein (HBXIP) is associated with a variety of tumors. The purpose of this study was to investigate the clinicopathological significance of HBXIP expression in pancreatic ductal adenocarcinoma (PDAC) and to explore its potential as a biomarker for PDAC. METHODS: Immunohistochemical (IHC) staining was performed on 126 PDAC tissues, 36 paraneoplastic tissues and 22 normal pancreatic tissues. The relationship between high levels of HBXIP expression and pathological features of PDAC patients was evaluated by chi-squared values. RESULTS: The positive rate of HBXIP protein in PDAC tissues was 85.7% (108/126), which was significantly higher than that of adjacent pancreatic tissue (41.7%, 15/36) and normal pancreas (18.2%, 4/22). In addition, strong positive expression of HBXIP was associated with tumor size, positive lymph node metastasis, clinical stage and 80-month overall survival. Patient's age, gender, degree of differentiation, Ki-67 expression index, and calcification were, however, not associated with high levels of HBXIP expression. CONCLUSIONS: We present association between HBXIP expression and the pathological features of patients with PDAC.

2 Article Transfer RNA demethylase ALKBH3 promotes cancer progression via induction of tRNA-derived small RNAs. 2019

Chen, Zhuojia / Qi, Meijie / Shen, Bin / Luo, Guanzheng / Wu, Yingmin / Li, Jiexin / Lu, Zhike / Zheng, Zhong / Dai, Qing / Wang, Hongsheng. ·Sun Yat-sen University Cancer Center; State Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine, Guangzhou 510060, China. · Department of Chemistry, The University of Chicago, 929 East 57th Street, Chicago, IL 60637, USA. · State Key Laboratory of Reproductive Medicine, Department of Histology and Embryology, Nanjing Medical University, Nanjing 211166, China. · School of Life Sciences, Sun Yat-sen University, Guangzhou 510006, China. · Department of Microbial and Biochemical Pharmacy, Guangdong Provincial Key Laboratory of New Drug Design and Evaluation, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China. ·Nucleic Acids Res · Pubmed #30541109.

ABSTRACT: Transfer RNA is heavily modified and plays a central role in protein synthesis and cellular functions. Here we demonstrate that ALKBH3 is a 1-methyladenosine (m1A) and 3-methylcytidine (m3C) demethylase of tRNA. ALKBH3 can promote cancer cell proliferation, migration and invasion. In vivo study confirms the regulation effects of ALKBH3 on growth of tumor xenograft. The m1A demethylated tRNA is more sensitive to angiogenin (ANG) cleavage, followed by generating tRNA-derived small RNAs (tDRs) around the anticodon regions. tDRs are conserved among species, which strengthen the ribosome assembly and prevent apoptosis triggered by cytochrome c (Cyt c). Our discovery opens a potential and novel paradigm of tRNA demethylase, which regulates biological functions via generation of tDRs.

3 Article Sensitive tumour detection and classification using plasma cell-free DNA methylomes. 2018

Shen, Shu Yi / Singhania, Rajat / Fehringer, Gordon / Chakravarthy, Ankur / Roehrl, Michael H A / Chadwick, Dianne / Zuzarte, Philip C / Borgida, Ayelet / Wang, Ting Ting / Li, Tiantian / Kis, Olena / Zhao, Zhen / Spreafico, Anna / Medina, Tiago da Silva / Wang, Yadon / Roulois, David / Ettayebi, Ilias / Chen, Zhuo / Chow, Signy / Murphy, Tracy / Arruda, Andrea / O'Kane, Grainne M / Liu, Jessica / Mansour, Mark / McPherson, John D / O'Brien, Catherine / Leighl, Natasha / Bedard, Philippe L / Fleshner, Neil / Liu, Geoffrey / Minden, Mark D / Gallinger, Steven / Goldenberg, Anna / Pugh, Trevor J / Hoffman, Michael M / Bratman, Scott V / Hung, Rayjean J / De Carvalho, Daniel D. ·Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada. · Lunenfeld-Tanenbaum Research Institute, Sinai Health System, Toronto, Ontario, Canada. · Memorial Sloan Kettering Cancer Center, New York, NY, USA. · Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada. · Genome Technologies, Ontario Institute for Cancer Research, Toronto, Ontario, Canada. · UMR_S 1236, Univ Rennes 1, Inserm, Etablissement Français du sang Bretagne, Rennes, France. · Department of Biochemistry and Molecular Medicine, UC Davis Comprehensive Cancer Center, Sacramento, CA, USA. · Division of Epidemiology, Dalla Lana School of Public Health, University of Toronto, Toronto, Ontario, Canada. · Fred Litwin Centre for Cancer Genetics, Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada. · Department of Surgery, Toronto General Hospital, Toronto, Ontario, Canada. · Department of Computer Science, University of Toronto, Toronto, Ontario, Canada. · Lunenfeld-Tanenbaum Research Institute, Sinai Health System, Toronto, Ontario, Canada. rayjean.hung@lunenfeld.ca. · Division of Epidemiology, Dalla Lana School of Public Health, University of Toronto, Toronto, Ontario, Canada. rayjean.hung@lunenfeld.ca. · Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada. ddecarv@uhnresearch.ca. · Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada. ddecarv@uhnresearch.ca. ·Nature · Pubmed #30429608.

ABSTRACT: The use of liquid biopsies for cancer detection and management is rapidly gaining prominence

4 Article Effects of miR-340 on hepatocellular carcinoma by targeting the DcR3 gene. 2018

Xie, Lijuan / Chen, Zhuo / Liu, Hongyu / Guan, Lianyue / Wang, Zhanpeng / Li, Wei. ·Department of Vascular Surgery, China-Japan Union Hospital of Jilin University, Changchun, China. · Department of Neurosurgery, China-Japan Union Hospital of Jilin University, Changchun, China. · Department of Hepatobiliary-Pancreatic Surgery, China-Japan Union Hospital of Jilin University, Changchun, China. · Department of Hepatobiliary-Pancreatic Surgery, China-Japan Union Hospital of Jilin University, Changchun, China. Electronic address: weili888@jlu.edu.cn. ·Dig Liver Dis · Pubmed #29311025.

ABSTRACT: In hepatocellular carcinoma (HCC), miR-340 plays a vital role in the regulation of tumor occurrence and deterioration, while DcR3 gene is involved in cancer cell proliferation and apoptosis. This study analyzed miR-340 in the serum of patients with HCC and healthy controls. Then, miR-340, DcR3, TGF-β1 and Smad2 expression were measured in HCC tissues and adjacent parts. Relationship between miR-340 and DcR3 was verified. Effects of miR-340 on human HepG2 cell proliferation and apoptosis were explored. miR-340, DcR3, TGF-β1, Smad2 mRNA and protein expression were also determined after miR-340 transfection. Compared with the control, miR-340 was significantly lower in the serum of the HCC patients (p < 0.01). miR-340 was lower in HCC tissues than in adjacent; however, DcR3, TGF-β1 and Smad2 were higher (p < 0.01). Furthermore, luciferase activity was significantly lower in the cells co-transfected with miR-340 mimics and DcR3-3'UTR-WT (p < 0.01), indicating that DcR3 was a target gene of miR-340. Moreover, decreased expression in DcR3, TGF-β1 and Smad2 was detected after miR-340 overexpression (p < 0.01), thus promoting apoptosis and blocking the proliferation of human HepG2 cells (p < 0.05). Furthermore, overexpression of DcR3 could activate the TGF-β1/Smad2 signal transduction pathway and increase the phosphorylation of Smad2. In conclusion, miR-340 plays a suppressive role in HCC development by targeting DcR3 and silencing the TGF-β1/Smad2 signaling pathway.

5 Article Two BRM promoter polymorphisms predict poor survival in patients with hepatocellular carcinoma. 2018

Pasic, Ivan / Wong, Kit M / Lee, Jonghun J / Espin-Garcia, Osvaldo / Brhane, Yonathan / Cheng, Dangxiao / Chen, Zhuo / Patel, Devalben / Brown, Catherine / Bucur, Roxana / Reisman, David / Knox, Jennifer J / Xu, Wei / Hung, Rayjean J / Liu, Geoffrey / Cleary, Sean P. ·Princess Margaret Cancer Centre, University Health Network, Toronto, Canada. · University of Toronto, Toronto, Canada. · Department of Medical Oncology, University of Washington, Seattle, Washington. · Lunenfeld Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada. · University of Florida, Gainesville, Florida. · Department of Surgery, Mayo Clinic College of Medicine, Rochester, Minnesota. ·Mol Carcinog · Pubmed #28892201.

ABSTRACT: Polymorphisms in the promoter of the BRM gene, a critical subunit of the chromatin remodeling SWI/SNF complex, have previously been implicated in risk and prognosis in Caucasian-predominant lung, head and neck, esophageal, and pancreatic cancers, and in hepatocellular cancers in Asians. We investigated the role of these polymorphisms in hepatocellular carcinoma (HCC) risk and prognosis. HCC cases were recruited in a comprehensive cancer center while the matched controls were recruited from family practice units from the same catchment area. For risk analyses, unconditional logistic regression analyses were performed in HCC patients and matched healthy controls. Overall survival analyses were performed using Cox proportional hazard models, Kaplan-Meier curves, and log-rank tests. In 266 HCC cases and 536 controls, no association between either BRM promoter polymorphism (BRM-741 or BRM-1321) and risk of HCC was identified (P > 0.10 for all comparisons). There was significant worsening of overall survival as the number of variant alleles increased: BRM-741 per variant allele adjusted hazards ratio (aHR) 5.77, 95% confidence interval (CI) 2.89-11.54 and BRM-1321 per variant allele aHR 4.09, 95%CI 2.22-7.51. The effects of these two polymorphisms were at least additive, where individuals who were double homozygotes for the variant alleles had a 45-fold increase in risk of death when compared to those who were double wild-type for the two polymorphisms. Two BRM promoter polymorphisms were strongly associated with HCC prognosis but were not associated with increased HCC susceptibility. The association was strongest in double homozygotes for the allele variants.

6 Article BRM polymorphisms, pancreatic cancer risk and survival. 2016

Segedi, Maja / Anderson, Laura N / Espin-Garcia, Osvaldo / Borgida, Ayelet / Bianco, Teresa / Cheng, Dangxiao / Chen, Zhuo / Patel, Devalben / Brown, M Catherine / Xu, Wei / Reisman, David / Gallinger, Steven / Cotterchio, Michelle / Hung, Rayjean / Liu, Geoffrey / Cleary, Sean P. ·Department of Surgery, University of British Columbia, Vancouver, BC, Canada. · Princess Margaret Cancer Centre-University Health Network-Ontario Cancer Institute, University of Toronto, Toronto, ON, Canada. · Mount Sinai Hospital-Lunenfeld Research Institute, Toronto, ON, Canada. · Medical Oncology, University of Florida, Gainesville, FL. · Prevention and Cancer Control, Cancer Care Ontario, Toronto, ON, Canada. · Princess Margaret Cancer Centre-University Health Network-Ontario Cancer Institute, University of Toronto, Toronto, ON, Canada. Geoffrey.Liu@uhn.ca. ·Int J Cancer · Pubmed #27487558.

ABSTRACT: Variant alleles of two promoter polymorphisms in the BRM gene (BRM-741, BRM-1321), create MEF2D transcription binding sites that lead to epigenetic silencing of BRM, the key catalytic component of the SWI/SNF chromatin remodeling complex. BRM suppression can be reversed pharmacologically.(1) Our group and others have reported associations with lung, head and neck, hepatocellular cancer risk,(1-3) and with lung and esophageal cancer prognosis (ASCO 2013; abstract 11057 & 4077). Herein, we assessed risk and survival associations with pancreatic cancer. A provincial population-based case-control study was conducted with 623 histologically confirmed pancreatic adenocarcinoma cases and 1,192 age/gender distribution-matched controls.(4) Survival of cases was obtained through the Ontario Cancer Registry. Logistic and Cox proportional hazard regression models were fitted, adjusting for relevant covariates. Median age was 65 y; 52% were male; Stage I (8%), II (55%), III (14%), IV (23%); 53% after curative resection, 79% after chemotherapy; and 83% had died. In the risk analysis, adjusted odds ratios (aOR) were 1.01 (95% CI: 0.1-2.0) and 0.96 (95% CI: 0.7-1.3) for the homozygotes of BRM-741 and BRM-1321, respectively; aOR of double-homozygotes was 1.11 (95% CI: 0.80-1.53), compared to the double-wildtype. For the survival analysis, adjusted hazard ratios (aHR) were 2.19 (95% CI: 1.9-2.5) for BRM-741 and 1.94 (95% CI: 1.7-2.2) for BRM-1321, per unit increase in variant alleles. Compared with the double-wildtype, aHR for carrying no, one, and two double-homozygotes were 2.14 (95% CI: 1.6-2.8), 4.17 (95% CI: 3.0-5.7), 8.03 (95% CI: 5.7-11.4), respectively. In conclusion, two functional promoter BRM polymorphisms were not associated with pancreatic adenocarcinoma risk, but are strongly associated with survival.