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作 者:Chen, Wen-Lian Wang, Yue-Ying Zhao, Aihua Xia, Li Xie, Guoxiang Su, Mingming Zhao, Linjing Liu, Jiajian Qu, Chun Wei, Runmin Rajani, Cynthia Ni, Yan Cheng, Zhen Chen, Zhu Chen, Sai-Juan[1] Jia, Wei[2,3]
机构地区:[1]Shanghai Jiao Tong Univ, Sch Med, State Key Lab Med Genom, Dept Hematol,Shanghai Inst Hematol,Rui Jin Hosp, Shanghai 200025, Peoples R China [2]Shanghai Jiao Tong Univ, Affiliated Peoples Hosp 6, Ctr Translat Med, Shanghai 200233, Peoples R China [3]Univ Hawaii, Ctr Canc, Honolulu, HI 96813 USA [4]Stanford Univ, Sch Med, Mol Imaging Program Stanford, Dept Radiol, Stanford, CA 94305 USA [5]Stanford Univ, BioX Program, Canary Ctr Stanford Canc Early Detect, Stanford, CA 94305 USA
出 处:《现代生物医学进展》2017年第6期I0001-I0002,共2页Progress in Modern Biomedicine
摘 要:近日,刊登在国际杂志Cancer Cell上的一项研究报告中,来自上海交通大学医学院等机构的研究人员通过研究发现了治疗急性髓性白血病(AML)的新型治疗靶点和新型疗法,急性髓性白血病是一种血液骨髓癌症,通常需要及时且积极的疗法对这种癌症进行治疗。Rapidly proliferating leukemic progenitor cells consume substantial glucose, which may lead to glucose insufficiency in bone marrow. We show that acute myeloid leukemia (AML) cells are prone to fructose utilization with an upregulated fructose transporter GLUTS, which compensates for glucose deficiency. Notably, AML patients with upregulated transcription of the GLUT5-encoding gene SLC2A5 or increased fructose utilization have poor outcomes. Pharmacological blockage of fructose uptake ameliorates leukemic phenotypes and potentiates the cytotoxicity of the antileukemic agent, Ara-C. In conclusion, this study highlights enhanced fructose utilization as a metabolic feature of AML and a potential therapeutic target.
关 键 词:CELL 白血病 治疗 疗法 急性 科学家 开发 上海交通大学
分 类 号:TP332[自动化与计算机技术—计算机系统结构]
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