【摘 要】
：
Introduction T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematologic malignancy accounting for 15% of pediatric and 25% of adult acute lymphoblastic leukemia (ALL) cases.With current
【机 构】
：
The University of Texas MD Anderson Cancer Center,Department of Hematopathology
论文部分内容阅读
Introduction T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematologic malignancy accounting for 15% of pediatric and 25% of adult acute lymphoblastic leukemia (ALL) cases.With current chemotherapies and transplantation therapy, there are still 25-50% T-ALL patients that suffer from relapse and have a poor outcome.MicroRNAs (miRNAs or miRs) are endogenous, small non-coding RNAs (containing about 22 nucleotides in length).miRs function at posttranscriptional level as negative regulators of gene expression and exert their regulatory function through binding to target mRNAs and silencing gene expression.To better understand the pathogenesis and develop the new therapeutic targets of T-ALL, we have developed a Pten tumor suppressor knockout T-ALL mouse model and profiled miRs from the mouse Pten deficient T-ALL.miR-26b was one of the miRs that were found down-regulated in the mouse Pten deficient T-ALL.Recent studies showed that the aberrant expression of rniR-26b is implicated in several types of cancer.The expression level of miR-26b and its role of in T-ALL, however, is unknown.We investigated if the expression level of miR-26b is aberrant in T-ALL and the effect of potentially altered expression on the growth of human T-ALL cells.
其他文献
Objective Elaborate evaluation of prognosis of T-cell lymphoma (TCL) is vital for current therapy and future stratified and individualized therapy.MicroRNAs (miRNAs) play important roles in cancer dev
Tight regulation of the cell cycle in hematopoietic stem cells (HSCs) is essential for maintaining their lifelong self-renewal capacity.Foxm1, a mammalian Forkhead Box M 1 protein, is known as a trans
目的 前期研究提示金属铜配合物可以特异性结合铜转运蛋白，下调其表达，减少了药物的流失，增强了药物对肿瘤细胞的敏感性。本研究目的主要是研究自主合成含硒铜配合物Se2Cu对白血病细胞的抑制作用及其可能的耐药机制。方法 采用CCK8检测含硒铜配合物Se2Cu对慢性粒细胞白血病K562细胞和耐药的K562R细胞的抑制作用；应用流式细胞术检测含硒铜配合物抑制白血病细胞生长的作用机制；由于铜配合物具有荧光，采
目的 探讨长链非编码RNA PVT1(lncRNA-PVT1)对急性早幼粒细胞白血病(APL)细胞株NB4增殖的影响及其相关分子机制.方法 通过实时定量PCR(qRT-PCR)的方法检测APL患者和健康人外周血白细胞、以及全反式维甲酸(ATRA)诱导NB4细胞分化前后的lncRNA-PVT1的表达水平；设计针对lncRNA-PVT1的siRNA,并转染NB4细胞,利用qRT-PCR检测siRNA的
研究目的 CFTR属于ATP结合(ABC)转运体超家族成员,是一种cAMP依赖的C1-通道,能够介导C1-和HCO3-的转运.近年研究发现CFTR不仅是一种阴离子通道蛋白,更可以作为调节器,通过蛋白之间的相互作用,调节其他蛋白的功能.本研究主要探讨CFTR在Ph+急性白血病的表达及信号调控网络中的作用,明确CFTR调控BCR-ABL的机制.研究方法 Western-blot法分析正常人呼吸道上皮细
目的 多发性骨髓瘤表现为恶性浆细胞在骨髓内的异常增殖。骨髓瘤的骨定位性质对骨髓瘤的临床表现与治疗都具有深远的影响。本项目从现象与机制两个方面探讨了巨噬细胞迁移抑制因子(MIF)对骨髓瘤骨定位的调控。方法 本项目采用了多种分子生物学方法。一些重要实验方法包括：生物信息学分析MIF表达与骨髓瘤临床因素(clinic factor)之间的相关性；定量PCR及免疫组化法确定MIF在骨髓瘤中的表达；实验鼠体
目的 探讨人叉头蛋白转录因子超家族O1 (FoxO1)在多发性骨髓瘤(Multiple Myeloma,MM)患者骨髓内皮细胞(Bone Marrow Endothelial Cell,BMEC)血管新生中的作用,为抗MM血管新生的研究提供新的靶点.方法 1.从MM患者骨髓中分离和培养内皮细胞；2.采用基因瞬时沉默技术在BMEC中敲除FoxO1基因,通过Q-PCR法和Western blot法,分
Acute myeloid leukemia (AML) is a group of heterogeneous hematopoietic malignancies sustained by a small population of leukemic stem cells (LSCs) that can resist treatment and act as barriers to cure.
目的 在肿瘤治疗中,如何选择具有高度选择性的抗癌药物是人们面临的巨大挑战。肿瘤微环境可激活肿瘤细胞内质网应激,肿瘤细胞随即产生未折叠蛋白反应作为一种适应性、保护性反应,也成为肿瘤细胞耐药的重要原因。筛选针对未折叠蛋白反应的新型药物有望为肿瘤治疗提供新思路。方法 我们采用细胞水平的未折叠蛋白反应抑制剂筛选模型对化合物进行筛选,筛选出候选化合物17＃。以2-脱氧葡萄糖模拟肿瘤低糖环境,通过Wester
Ibrutinib, an irreversible Brutons tyrosine kinase (BTK) inhibitor, has induced significant clinical responses in B-cell malignancies.Our study is to elucidate its actions on diffuse large B-cell lymp