MLL‐ELL fusion gene in an acute myelomonocytic leukemia patient transformed from acute promyelocytic leukemia

We report an extremely rare case of acute myelomonocytic leukemia (M4) with an MLL‐ELL fusion gene lacking the PML‐RARα rearrangement that transformed from hypergranular acute promyelocytic leukemia (APL) without showing any karyotypic evolution. The treatment was effective with chemotherapy for M4 and idarubicin plus a cytarabine‐based chemotherapy protocol without ATRA.     

ELL基因在前列腺癌组织中的表达及其意义

目的分析 ELL基因在人类前列腺癌组织中的表达情况,探讨其在前列腺癌发生发展中的作用.方法收集45例前列腺癌组织、15例良性前列腺增生组织和15例正常前列腺组织,提取总 RNA,应用 qRT-PCR检测 ELL mRNA的表达情况,分析其与前列腺癌分级的关系.结果前列腺癌组织中 ELL mRNA 的表达量明显低于良性前列腺增生组织和正常前列腺组织(P＜0．05),而良性前列腺增生组织与正常前列腺组织间差异无统计学意义.随着前列腺癌Gleason评分的升高,ELL mRNA的表达呈下降趋势(P＜0．05).结论 ELL 基因在前列腺癌组织中呈低表达,其表达与前列腺癌的分级密切相关,提示其可能在前列腺癌的发生发展中发挥重要作用.     

ELL慢病毒表达载体的构建及其感染前列腺癌PC3细胞的研究

目的构建ELL基因的慢病毒表达质粒,探讨其感染人前列腺癌PC3细胞的可行性。方法将含有全长ELL的质粒和慢病毒表达载体经双酶切后连接,构建成重组慢病毒载体质粒pCDH1-MCS1-EF1-copGFP—ELL。对慢病毒载体质粒进行双酶切和测序鉴定后,制备包装病毒并转染人前列腺癌细胞系PC3。结果慢病毒载体质粒pCDH1-MCS--EF1-copGFP—ELL的酶切和测序结果与预计的序列一致。慢病毒感染人前列腺癌PC3细胞后能稳定高表达ELL。结论成功构建了ELL的慢病毒表达载体,ELL可被成功转染人人前列腺癌细胞。     

ELL2在人成骨肉瘤中的表达及对MG-63细胞增殖的影响

目的:研究ELL2在人成骨肉瘤中的表达情况以及其对人成骨肉瘤细胞增殖的影响.方法:运用RT-PCR检测ELL2在人成骨肉瘤组织及其正常毗邻组织中的表达,RT-PCR及Western-blot检测ELL2在人成骨肉瘤细胞系及人正常成骨细胞系中的表达.构建ELL2过表达载体,MTT和细胞计数试验检测过表达ELL2对人成骨肉瘤细胞系MG-63增殖的影响.结果:ELL2在人成骨肉瘤组织中的表达显著低于其正常毗邻组织(P=0.001).ELL2在人成骨肉瘤细胞系中的表达相比于人正常成骨细胞系明显下调(P<0.05).过表达ELL2能够显著抑制MG-63细胞的增殖(P<0.05).结论:ELL2在人成骨肉瘤中表达下调,其过表达能够抑制肿瘤细胞的增殖.     

Apoptosis induction and growth suppression by U19/Eaf2 is mediated through its ELL-binding domain

BACKGROUND: U19/Eaf2 is an androgen-response gene and its downregulation is frequently observed in advanced human prostate cancer. U19/Eaf2 interacts with ELL, a fusion partner of MLL in the (11;19) (q23;p13.1) translocation in acute myeloid leukemia. U19/Eaf2 overexpression induces apoptosis and suppresses xenograft tumor growth. METHODS: Transfection and colony formation were used to assay for apoptosis and growth suppression of various U19/Eaf2 mutants. Co-immunoprecipitation was performed to test the interaction between the U19/Eaf2 constructs and ELL. RESULTS: The region of U19/Eaf2 essential for apoptosis and growth suppression was mapped to amino acids 68-113. This region was necessary and sufficient for binding ELL. Co-expression of U19/Eaf2 and ELL in 293 cells lead to significant increase in cell death and growth suppression. CONCLUSIONS: These observations argue that the interaction with ELL is essential for the induction of apoptosis and growth suppression by U19/Eaf2.     

Revisiting the evolution of gonadotropin-releasing hormones and their receptors in vertebrates: secrets hidden in genomes

Gonadotropin-releasing hormone (GnRH) and its G protein-coupled receptor, GnRHR, play a pivotal role in the control of reproduction in vertebrates. To date, many GnRH and GnRHR genes have been identified in a large variety of vertebrate species using conventional biochemical and molecular biological tools in combination with bioinformatic tools. Phylogenetic approaches, primarily based on amino acid sequence identity, make it possible to classify these multiple GnRHs and GnRHRs into several lineages. Four vertebrate GnRH lineages GnRH1, GnRH2, GnRH3, and GnRH4 (for lamprey) are well established. Four vertebrate GnRHR lineages have also been proposed—three for nonmammalian GnRHRs and mammalian GnRHR2 as well as one for mammalian GnRHR1. However, these phylogenetic analyses cannot fully explain the evolutionary origins of each lineage and the relationships among the lineages. Rapid and vast accumulation of genome sequence information for many vertebrate species, together with advances in bioinformatic tools, has allowed large-scale genome comparison to explore the origin and relationship of gene families of interest. The present review discusses the evolutionary mechanism of vertebrate GnRHs and GnRHRs based on extensive genome comparison. In this article, we focus only on vertebrate genomes because of the difficulty in comparing invertebrate and vertebrate genomes due to their marked divergence.