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Pancreatic Neoplasms: HELP
Articles by X. F. Zhang
Based on 2 articles published since 2010
(Why 2 articles?)

Between 2010 and 2020, X. F. Zhang wrote the following 2 articles about Pancreatic Neoplasms.
+ Citations + Abstracts
1 Article Concentration changes in gemcitabine and its metabolites after hyperthermia in pancreatic cancer cells assessed using RP-HPLC. 2019

Jin, H B / Lu, L / Xie, L / Yang, J F / Zhang, X F / Ma, S L. ·Department of Gastroenterology, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, 310006 China. · 0000 0004 1759 700X · grid.13402.34 ·Cell Mol Biol Lett · Pubmed #31131010.

ABSTRACT: Background: Gemcitabine (2',2'-difluoro-2'-deoxycytidine;dFdC) is a first-line chemotherapy drug for pancreatic cancer. Recently, a synergistic anti-tumor treatment of dFdC and hyperthermia has achieved good clinical results, but there are few reports on the molecular mechanism influenced by hyperthermia. This study is an initial exploration of the effects of hyperthermia on changes in the concentration of dFdC and its metabolites in pancreatic cancer cells. The aim is to provide a theoretical basis for clinical detection and pharmacokinetic research. Methods: PANC-1 cells at logarithmic growth phase were used as the experimental object. The MTT assay was performed to determine the half maximal inhibitory concentration (IC Results: We found that 41 °C and 43 °Chyperthermia gave rise to a decrease in dFdC and dFdU content. At 41 °C, the levels respectively fell to 9.28 and 30.93% of the baseline, and at 43 °C, to 24.76 and 57.80%, respectively. The dFdCTP content increased by 21.82% at 41 °C and 42.42% at 43 °C. Conclusion: The two heat treatments could alter the mechanism of dFdC metabolism in PANC-1 cells. The effect of 43 °C hyperthermia is more significant. Our observations may be instrumental to explaining the higher anti-tumor efficacy of this combination therapy.

2 Article Effect of inhibition of MEK pathway on 5-aza-deoxycytidine-suppressed pancreatic cancer cell proliferation. 2013

Wang, X / Wang, H / Jiang, N / Lu, W / Zhang, X F / Fang, J Y. ·Department of Gastroenterology Medicine, First People's Hospital of Hangzhou, Hangzhou Medical School, Nanjing University, Hangzhou, Zhejiang, China. ·Genet Mol Res · Pubmed #24301926.

ABSTRACT: Pancreatic adenocarcinoma is a lethal disease because it is inoperable at the time of diagnosis. Therefore, the search for new therapeutic approaches is critical. The abnormal expression of the mitogen-activated protein kinase/extracellular signal-regulated kinase (MEK) pathway and alteration in epigenetic modification (DNA methylation and acetylation of histones) is a common feature in the majority of human pancreatic adenocarcinomas. Because DNA methyltransferase levels are regulated by the MEK pathway, we examined the effects of an MEK inhibitor, PD98059, on the action of DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine (5-aza-dC), the epigenetic agent in the pancreatic cell line CFPAC1. Our results showed that PD98059 significantly potentiated the capability of 5-aza-dC to induce a cessation of cell proliferation concomitant with cell cycle arrest. We also observed an increase in tumor suppressor gene expression associated with the efficacy of treatment with PD98059 and 5-aza-dC. Further studies explored the molecular mechanisms by which 5-aza-dC induced the expression of p21(WAF1). We found that 5-aza-dC induced acetylation of histone H3 on the p21(WAF1) gene promoter and demethylation status on the p21(WAF1) gene promoter region. These effects were strikingly enhanced by the concomitant blockade of the MEK pathway. Furthermore, knockdown of p21(WAF1) by small interfering RNA rescued human pancreatic cancer cells from 5-aza-dC-mediated growth inhibition. Taken together, our results show that the MEK inhibitor enhanced the effects of 5-aza-dC in human pancreatic cancer cells. These results suggest that the MEK signal pathway may be a potential target for pancreatic cancer therapy.