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Pancreatic Neoplasms: HELP
Articles by Bowen Gao
Based on 2 articles published since 2010
(Why 2 articles?)
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Between 2010 and 2020, Bo Gao wrote the following 2 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Review The potential role of 2019

Liu, Xiao-Bo / Gao, Zi-Ye / Sun, Chuan-Tao / Wen, Hui / Gao, Bo / Li, Sheng-Bao / Tong, Qiang. ·Department of Gastroenterology, Taihe Hospital, Hubei University of Medicine, 32 south renmin road, Shiyan, Hubei 442000 People's Republic of China. · Department of Oncology, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000 Hubei China. · Department of Laboratory Medicine, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000 Hubei China. ·Infect Agent Cancer · Pubmed #31516546.

ABSTRACT: Bacterial infection may be involved in the entire process of tissue carcinogenesis by directly or indirectly affecting the occurrence and development of tumors.

2 Article HEATR1 Negatively Regulates Akt to Help Sensitize Pancreatic Cancer Cells to Chemotherapy. 2016

Liu, Tongzheng / Fang, Yuan / Zhang, Haoxing / Deng, Min / Gao, Bowen / Niu, Nifang / Yu, Jia / Lee, SeungBaek / Kim, JungJin / Qin, Bo / Xie, Fang / Evans, Debra / Wang, Liewei / Lou, Wenhui / Lou, Zhenkun. ·Division of Oncology Research, Department of Oncology, Mayo Clinic, Rochester, Minnesota. · Department of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China. · Division of Oncology Research, Department of Oncology, Mayo Clinic, Rochester, Minnesota. School of Life Sciences, Southwest University, Chongqing, China. · Division of Clinical Pharmacology, Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, Minnesota. · School of Life Sciences, Southwest University, Chongqing, China. · Department of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China. lou.zhenkun@mayo.edu lou.wenhui@zs-hospital.sh.cn. · Division of Oncology Research, Department of Oncology, Mayo Clinic, Rochester, Minnesota. lou.zhenkun@mayo.edu lou.wenhui@zs-hospital.sh.cn. ·Cancer Res · Pubmed #26676747.

ABSTRACT: Elucidating mechanisms of chemoresistance is critical to improve cancer therapy, especially for the treatment of pancreatic ductal adenocarcinoma (PDAC). Genome-wide association studies have suggested the less studied gene HEAT repeat-containing protein 1 (HEATR1) as a possible determinant of cellular sensitivity to different chemotherapeutic drugs. In this study, we assessed this hypothesized link in PDAC, where HEATR1 expression is downregulated significantly. HEATR1 silencing in PDAC cells increased resistance to gemcitabine and other chemotherapeutics, where this effect was associated with increased AKT kinase phosphorylation at the Thr308 regulatory site. Mechanistically, HEATR1 enhanced cell responsiveness to gemcitabine by acting as a scaffold to facilitate interactions between AKT and the protein phosphatase PP2A, thereby promoting Thr308 dephosphorylation. Consistent with these findings, treatment with the AKT inhibitor triciribine sensitized HEATR1-depleted PDAC cells to gemcitabine, suggesting that this therapeutic combination may overcome gemcitabine resistance in patients with low HEATR1 expression. Clinically, we found that HEATR1 downregulation in PDAC patients was associated with increased AKT phosphorylation, poor response to tumor resection plus gemcitabine standard-of-care treatment, and shorter overall survival. Collectively, our findings establish HEATR1 as a novel regulator of AKT and a candidate predictive and prognostic indicator of drug responsiveness and outcome in PDAC patients.