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作 者:Yuriko Saiki Shuto Hirota Akira Horii
机构地区:[1]Department of Molecular Pathology,Tohoku University School of Medicine,Sendai,Miyagi 980-8575,Japan [2]Office of Medical Education,Tohoku University School of Medicine,Sendai,Miyagi 980-8575,Japan [3]Saka General Hospital,Shiogama,Miyagi 985-0024,Japan
出 处:《Cancer Drug Resistance》2020年第4期819-831,共13页癌症耐药(英文)
摘 要:Gemcitabine is a cytidine analogue frequently used in the treatment of various cancers.However,the development of chemoresistance limits its effectiveness.Gemcitabine resistance is regulated by various factors,including aberrant genetic and epigenetic controls,metabolism of gemcitabine,the microenvironment,epithelial-to-mesenchymal transition,and acquisition of cancer stem cell properties.In many situations,results using cell lines offer valuable lessons leading to the first steps of important findings.In this review,we mainly discuss the factors involved in gemcitabine metabolism in association with chemoresistance,including nucleoside transporters,deoxycytidine kinase,cytidine deaminase,and ATP-binding cassette transporters,and outline new perspectives for enhancing the efficacy of gemcitabine to overcome acquired chemoresistance.
关 键 词:GEMCITABINE CHEMORESISTANCE deoxycytidine kinase human equilibrative nucleoside transporter 1 cytidine deaminase ATP-binding cassette transporters METABOLISM
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