...
首页> 外文期刊>Haematologica >Inhibitors of poly ADP-ribose polymerase (PARP) induce apoptosis of myeloid leukemic cells: potential for therapy of myeloid leukemia and myelodysplastic syndromes
【24h】

Inhibitors of poly ADP-ribose polymerase (PARP) induce apoptosis of myeloid leukemic cells: potential for therapy of myeloid leukemia and myelodysplastic syndromes

机译:聚ADP-核糖聚合酶的抑制剂(PARP)诱导骨髓性白血病细胞凋亡:骨髓白血病治疗的潜力和髓细胞转化综合征

获取原文
   

获取外文期刊封面封底 >>

       

摘要

In the original article, there was a mistake in Figure 3D as published. In this instance, the annexin V fluorescence-activated cell sorting (FACS) image for Figure 1B (top right) had been unintentionally duplicated and substituted for the annexin V FACS image in Figure 3D (top left). As it is an untreated drug control rather than drug test additions, no scientific benefit or advantage interpretation could be made by duplicating the data here. The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The amended Figure 3 is attached. An incorrect version of Figure 3 appared in the May 2009 Issue on page 644. The correct version of Figure 3 is published on this page. Figure 3. The effect on leukemic cells of the PARP inhibitor, KU in combination with non-cytotoxic concentrations of 5’-aza-2’-dCR and/or HDAC inhibitor. (A) The effect on primary acute myeloid leukemia (AML) cells of the PARP inhibitor, KU in combination with the HDAC inhibitor, MS275 and with 5’-aza-2’-dCR. KU was added at variable concentrations to Patient 2 continuously for 5 days with 50 nM MS275 and 200 nM 5’-aza-2’-dCR or KU alone and then analyzed by flow cytometry. The apoptotic index (Sub-G1population as a fraction of sub-G1+ G1 populations is shown in the right inset). (B) Trypan blue exclusion assays were used to determine cell survival in primary AML cells of Patient 2 exposed to KU, MS275 and 5’-aza-2’-dCR. Exposure to 50 nM MS275 and 200 nM 5’-aza-2’-dCR with varying concentrations of KU was continuous for 5 days in AML cells of Patient 1 and AML cells of Patient 2 cells. KU + MS275 (triangles), 5’-aza-2’-dCR + KU + MS275 (diamonds), KU alone (squares). (C) P39 cells were cultured in 1 mM KU, 1 mM KU + 100 nM MS275 or left untreated for 7 days. At 7 days cells were cytospun onto slides and stained with May-Grumwald stain. Images were taken at 40X magnification. (D) 1 mM KU, 100 nM MS275 and 250 nM 5’-aza-2’-CdR were added as indicated to P39 for 7 days before being treated with annexin V-FITC (FL-1, X-axis) and propidium iodide (FL-2, Y-axis). The figures show the percentage of early and late apoptotic cells in the population.
机译:在原始文章中,如发布的图3D存在错误。在这种情况下,图1B的附睾v荧光激活的细胞分选(FACS)图像(右上)无意中复制并取代图3D中的附膜蛋白V facs图像(左上角)。由于它是未经治疗的药物控制而不是药物测试添加,可以通过在此复制数据来进行科学效益或优势解释。作者对这个错误而道歉,并说明这不会以任何方式改变文章的科学结论。修订的图3是附加的。第644页的2009年5月发布中可能在图3中进行了不正确的版本。图3的正确版本在此页面上发布。图3.对PARP抑制剂的白血病细胞的影响,Ku与5'-AZA-2'-DCR和/或HDAC抑制剂的非细胞毒性浓度组合。 (a)对PARP抑制剂的原发性急性髓细胞白血病(AML)细胞与HDAC抑制剂,MS275和5'-AZA-2'-DCR组合的影响。 Ku以可变浓度加入到患者2中,用50nm MS275和200nM 5'-AZA-2'-DCR或Ku单独使用5天,然后通过流式细胞术分析。凋亡指数(Sub-G1作为次G1 + G1种群的分数显示在右侧插入中)。 (b)用于测定暴露于Ku,MS275和5'-AZA-2'-DCCR的患者2的母AML细胞中初级AML细胞中的细胞存活的细胞存活。暴露于50nm的MS275和200nm 5'-Aza-2'-DCR,其具有不同浓度的Ku在患者1和患者2细胞的AML细胞的AML细胞中连续5天。 KU + MS275(三角形),5'-AZA-2'-DCR + KU + MS275(钻石),单独的KU(正方形)。 (c)将P39细胞在1mm Ku,1mm Ku + 100nm MS275中培养或未治疗7天。在7天内将细胞呈Cytospun载有载玻片并用5月Grumwald染色染色。图像以40倍放大率拍摄。 (D)1mm Ku,加入100nm MS275和250nm 5'-AZA-2'-CDR,如P39用膜蛋白V-FITC(FL-1,X轴)和丙醇处理碘化物(FL-2,Y轴)。这些数字显示人口中早期和晚期凋亡细胞的百分比。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号