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Inhibition of glucuronidation in pancreatic cancer improves gemcitabine anticancer activity

查看全文 作  者:Nicolas Alejandro [1,2]Fraunhoffer;Analía Meilerman [1]Abuelafia;Brice [1]Chanez;Martin [1,4]Bigonnet;Odile [1]Gayet;Julie [1]Roques;Eduardo [2,3]Chuluyan;Nelson [1]Dusetti;Juan [1]Iovanna 高影响力作者 机构地区:[1]Cancer Research Center of Marseille,Inserm,Paoli-Calmettes Institut,Aix-Marseille University,Scientific and Technological Park of Luminy,Marseille 13288,France;[2]Buenos Aires University,Center for Pharmacological and Botanical Studies,Faculty of Medicine,National Council for Scientific and Technical Research,Buenos Aires,C1121ABG,Argentina;[3]Buenos Aires University,Faculty of Medicine,Department of Microbiology,Parasitology and Immunology,Buenos Aires C1121ABG,Argentina;[4]Predicting Med,Scientific and Technological Park of Luminy,Marseille 13288,France高影响力机构 出  处:《Cancer Communications》索引2022年第42卷第11期,共5页高影响力期刊 基  金:supported by the National Cancer Institute(Grants number 2018-078,2019-037, 2018-079),Canceropole Provence-Alpes-Côte d’Azur,Amidex Foundation and the national institute of health and medical research. 摘  要:Dear Editor,Pancreatic ductal adenocarcinoma(PDAC)treatment is focused on two regimens.The polychemotherapy,FOLFIRINOX(folinic acid,fluorouracil,irinotecan,oxali-platin),is used in patients with good health conditions[1],while gemcitabine,as monotherapy,in patients with poor health conditions[2–4].Gemcitabine resistance-associated pathways have been targeted to sensitize cancer cells,but the results were disappointing.Using a transcrip-tomic bioinformatics analysis combined with biological validation,we showed that glucuronidation was associ-ated with the gemcitabine resistance in PDAC,and its inhibition could switch tumors from resistant to sensitive. 关 键 词:GEMCITABINE cancer CHEMOTHERAPY
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