| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Outline of Final Research Achievements |
The main treatment of leukemia is chemotherapy using antitumor drugs, but the acquisition of drug resistance often makes treatment continuation impossible. The mechanism of acquired drug resistance must be elucidated. We focused on glycan structures on cell-membrane proteins. A leukemia cell line (CEM) was selected for acquired drug resistance against an antitumor drug (dEpoB), and glycan structures on the cell-membrane proteins was analyzed. The resistant cell line (CEM/dEpoB) showed a significant decrease of 2-6 sialylated N-glycans. The reduction was cause of 2-6 sialyltransferase 1 (ST6GAL1) gene. To ascertain the cause-and-effect relationship between reduction of 2-6 sialylated N-glycans and acquired drug resistance, we knock-downed and transfected the ST6GAL1 gene. The CEM with the knock-down ST6GAL1 gene showed acquired drug resistance. This result suggests that reduction in the 2-6 sialylation could be the cause of dEpoB-resistance acquisition.
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