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- 白血病細胞株K562malignant myeloid cell lines K562
- GP-7抑制多藥耐藥白血病細胞株K562/ADM的作用優(yōu)于依托泊苷。Its inhibitory effect on K562/ADM cells is superior to etoposide.
- sFLT-1明顯抑制白血病細胞株K562及HL-60的生長(cháng),并且隨著(zhù)sFLT-1濃度的增加,其抑制率增加,以用藥后48小時(shí)抑制作用最明顯。sFLT-1 could effectively inhibit the growth of K562 and HL60 cell lines in dose-dependent manner.
- L-1時(shí)作用則相反。 結論GP-7可抑制多藥耐藥白血病細胞株K562/ADM的增殖,誘導細胞凋亡。CONCLUSION GP-7 may inhibit multidrug-resistant leukemia K562/ADM cells proliferation and induce apoptosis.
- 細胞株K562cell line K562
- 阿糖胞苷體外對人白血病細胞株HL-60細胞增殖抑制和誘導凋亡的相關(guān)性研究Study on the proliferation inhibition and apoptosis induction of Ara-C on treatment HL-60 in vitro
- 重組人IL-2激活外周血干細胞移植物的抗白血病細胞毒作用Anti-leukemia cytotoxicity of peripheral blood stem cell grafts activated by rhIL-2
- 細胞株cell strain
- 白血病細胞抗原leukemia cell antigen
- 人淋巴因子激活的殺傷細胞對肝癌細胞株凋謝作用的觀(guān)察A Observaion of Apoptoisi of Liver Cancer Cells Induced by Human LAK Cells
- 白血病細胞leukemia cell
- 復方藤梨根制劑體外對MDR細胞株K562/ADR和K562/VCR細胞積聚和外排阿霉素(ADR)的影響研究The study of effects on accumulation and efflux of intracellular adrimycine with FFTLG for multidrug resistant cell lines K562/ADR and K562/VCR in vitro
- 白血病細胞浸潤leukemia myelosis
- T24細胞株T24 Cell lines
- 紅白血病細胞K562Erythroleukemia K562 cells
- K562／A02細胞株K562/A02 cell line
- 非細胞毒性劑量的三氧化二砷和苦參堿均可部分逆轉有多藥耐藥表型的細胞株K562/ADM對阿霉素的耐藥J險，二者聯(lián)合應用效果優(yōu)于單獨應用，具有協(xié)同作用。K562/ADM had no drug resistance to As2O3 and matrine.
- 從病人體內分離培養的CIK細胞，在體外有強的殺傷K562細胞和裂解髓系白血病細胞的作用；CIK cells generated from patients could kill K562 cells and lysis myeloid leukemia cells in vitro.
- K562／AO2細胞株K5 6 2/AO2 cell strain
- 轉錄因子Sp1、Sp3對K562白血病細胞增殖、凋亡及耐藥性影響的研究Transcription Factors Sp1 and Sp3 Influence K562 Leukemia Cell Proliferation, Apoptosis and Drug Resistance
