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Pancreatic Neoplasms: HELP
Articles by F. Liu
Based on 2 articles published since 2010
(Why 2 articles?)
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Between 2010 and 2020, F. Liu wrote the following 2 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article [Multidisciplinary treatment and survival analysis for 497 cases of pancreatic cancer with liver metastases]. 2016

Ouyang, H H / Pan, Z Y / Ma, W D / Zhao, L J / Zhang, T / Liu, F / Quan, M M. ·Tianjin Medical University Cancer Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin 300060, China. ·Zhonghua Yi Xue Za Zhi · Pubmed #26875916.

ABSTRACT: OBJECTIVE: To explore the multidisciplinary therapeutic mode, clinical effect and prognostic factors of pancreatic cancer with liver metastases (PCLM). METHODS: We retrospectively selected 497 consecutive patients with PCLM who were pathologically diagnosed and treated at Tianjin Medical University Cancer Hospital, from January, 2000 to December, 2012. Clinical characteristics, treatment modality, survival condition and factors associated with prognosis of these cases were analyzed, and efficacy of multidisciplinary treatment model was evaluated. RESULTS: Of these patients, the male/female ratio was 1.85∶1, with a median age of 59. A total of 358 (72.0%) cases had synchronous liver metastases, and 173 (34.8%) cases complicated with extrahepatic metastases. The 0.5, 1, 3, 5 year survival rates of 497 patients were 44.1%, 19.7%, 3.2% and 2.2%, respectively, with a median survival (MS) of 5.4 months. Patients who were treated with 3 or more approaches (including surgery, chemotherapy, radiation therapy, interventional therapy, and physiotherapy) had a longer median survival time than patients treated with 2 or only 1 approach (MS: 8.6 vs 5.2 vs 4.6 months, P< 0.001). Multivariate analysis for clinical features and treatment modality showed that age, weight loss, ascites, karnofsky performance score (KPS), primary site resection, albumin, carbohydrate antigen (CA) 19-9, resection of liver metastases, radiation therapy and systemic chemotherapy were prognostic variables with statistical significance. CONCLUSIONS: PCLM is a refractory malignant tumor. Age >60, weight loss (≥10% within 3 months), ascites, KPS <80, albumin<35 g/L, and CA19-9 ≥500 U/ml were the most relevant predictors of poor survival. Multimodal treatment using curative resection of pancreatic cancer and/or liver metastases, systemic chemotherapy and radiation therapy may improve the prognosis and survival rate sufficiently.

2 Article Rasfonin, a novel 2-pyrone derivative, induces ras-mutated Panc-1 pancreatic tumor cell death in nude mice. 2014

Xiao, Z / Li, L / Li, Y / Zhou, W / Cheng, J / Liu, F / Zheng, P / Zhang, Y / Che, Y. ·Beijing Institute of Pharmacology and Toxicology, Beijing 100850, China. · 1] Beijing Institute of Pharmacology and Toxicology, Beijing 100850, China [2] Department of Pharmacology, Logistics College of Chinese People's Armed Police Forces, Tianjin, China. ·Cell Death Dis · Pubmed #24853419.

ABSTRACT: Rasfonin is a novel 2-pyrone derivative reported to induce apoptosis in ras-dependent cells. In this study, its effects on ras-mutated pancreatic cancer cells were investigated in vitro and in vivo. Two human pancreatic cancer cell lines Panc-1 (mutated K-ras) and BxPC-3 (wild-type K-ras) were selected to test the effects of rasfonin on cell proliferation, clone formation, migration and invasion in vitro. Immunoblotting was used to detect the expressions of EGFR-Ras-Raf-MEK-ERK signaling pathway proteins. Ras activity was measured using a pull-down ELISA kit and guanine exchange factor (GEF)/GTPase-activating proteins (GAP) activity was measured by [(3)H]-GDP radiometric ligand binding. For an in vivo study, CD1 nude mice bearing Panc-1 cells were treated with rasfonin or Salirasib (FTS). We found that rasfonin suppressed proliferation more strongly in Panc-1 cells (IC50=5.5 μM) than BxPC-3 cells (IC50=10 μM) in vitro. Clone formation, migration and invasion by Panc-1 cells were also reduced by rasfonin. Rasfonin had little effect on the farnesylation of Ras, but it strongly downregulated Ras activity and consequently phosphorylation of c-Raf/MEK/ERK. Further experiments indicated that rasfonin reduced Son of sevenless (Sos1) expression but did not alter GEF and GAP activities. The in vivo experiments also revealed that rasfonin (30 mg/kg) delayed the growth of xenograft tumors originating from Panc-1 cells. Tumor weight was ultimately decreased after 20 days of treatment of rasfonin. Rasfonin is a robust inhibitor of pancreatic cancers with the K-ras mutation. The reduction of Sos1 expression and the consequently depressed Ras-MAPK activity could be important in its anticancer activity.