The c-myc coding DNA sequences of cyprinids （Teleostei： Cypriniformes）： Implications for phylogeny

The family Cyprinidae is one of the largest fish families in the world, which is widely distributed in East Asian, with obvious difference in characteristic size among species. The phylogeneUc analysis of cyprinid taxa based on the functionally important genes can help to understand the speciation and functional divergence of the Cyprinidae. The c-myc gene is an important gene regulating individual growth. In the present study, the sequence variations of the cyprinid c-myc gene and their phylogenetic significance were analyzed. The 41 complete sequences of the c-myc gene were obtained from cyprinids and outgroups through PCR amplification and clone. The coding DNA sequences of the c-myc gene were used to infer molecular phylogenetic relationships within the Cyprinidae. Myxocyprinus asiaticus （Catostomidae）, Misgurnus anguillicaudatus （CobiUdae） and Hemimyzon sinensis （Homalopteridae） were assigned to the outgroup taxa. Phylogenetic analyses using maximum parsimony （MP）, maximum likelihood （ML）, and Bayesian retrieved similar topology. Within the Cyprinidae, Leuciscini and Barbini formed the monophyletic lineage respectively with high nodal supports. Leuciscini comprises Xenocyprinae, CuItrinae, East Asian species of Leuciscinae and Danioninae, Gobioninae and Acheilognathinae, and Barbini contains Schizothoracinae, Barbinae, Cyprininae and Labeoninae. Danio rerio, D. myersi and Rasbora trilineata were supposed to separate from Leuciscinae and Barbini and to form another lineage. The positions of some Danioninae species were still unresolved. Analyses of both amino acid variation with parsimony information and two high variation regions indicated that there is no correlation between variations of single amino acid or high variation regions and characteristic size of cyprinids. In addition, the species with smaller size were usually found to be basal within clades in the tree, which might be the results of the adaptation to the primitive ecology and survival pressure.     

新疆卡波氏肉瘤中c-myc、14-3-3β的表达

为探讨原癌基因c-myc、14-3-3β在新疆卡波氏肉瘤中的表达及意义,应用免疫组织化学Envision二步法检测新疆14例卡波氏肉瘤及对照组12例健康人正常皮肤组织内c-myc,14-3-3β的表达水平,结果显示：卡波氏肉瘤组织c-myc、14-3-3β蛋白均呈胞浆阳性,所有病例均呈阳性表达（14/14）,阳性率均为100%;c-myc蛋白在正常皮肤组织中多数病例呈阴性表达（3/12）,阳性率为25%,14-3-3β蛋白在正常皮肤组织中多数病例呈阴性表达（2/12）,阳性率为16.7%,c-myc、14-3-3β蛋白在KS中的表达明显高于在正常皮肤组织中的表达,差异均有统计学意义（P〈0.01）。表明：c-myc1、4-3-3β蛋白的异常表达在KS的发展过程中可能发挥了重要作用。     

敏感和抗性的白血病HL60细胞对staurosporine诱导凋亡的不同反应(英)

用对蛋白激酶具有强烈抑制、作用广泛的抑制剂staurosporine（Sta）,研究敏感和抗三尖杉酯碱的人白血病HL60细胞中凋亡和多药抗药性的关系．Sta均能诱导2种细胞发生典型的凋亡,但抗性细胞发生凋亡需更长的时间,凋亡的细胞数减少．Sta增加柔红霉素在抗性细胞内的积聚,说明其能逆转多药抗药性．在抗性细胞凋亡过程中,mdrl基因表达没有变化,c-myc基因表达稍有增加．结果显示：Sta能诱导敏感和抗三尖杉酯碱的HL60细胞发生凋亡,mdrl基因表达与凋亡过程无关．     

K252a: A new blocker of the cell-cycle at G1 phase in a human hepatoma cell line

The administration of 200 nM K252a to HuH7 suppressed the proliferation of the cells almost completely. The uptake of [³H]thymidine was inhibited, and flow cytometry revealed only one peak at 2C on day 3 after treatment with 100 nM K252a. The expression of proto-oncogene c-myc was not reduced. Despite the blockage at G1, both the size of the cells and the amount of cell protein had increased by 4 times by day 3 after treatment with K252a, while the cells secreted albumin and -fetoprotein into the medium as usual. These results show that K252a can increase the cell size of HuH7 without losing its function by blocking the cell cycle at G1 phase.     

螺旋藻藻蓝蛋白对人血癌细胞K562生长的影响

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缺氧环境下三氧化二砷对人肝癌HepG2细胞c-myc 表达的影响

目的：探讨缺氧环境下三氧化二砷（As20 3）对体外培养的人肝癌HepG2细胞c-myc蛋白表达的影响.方法：用氯化钴（CoC l2） 创造缺氧微环境,设常氧组、缺氧组及缺氧加药物组,用免疫细胞化学法观察4.0umol/L As203作用HepG2细胞48h后c-myc蛋白表达的影响.结果：常氧环境下c-myc蛋白呈弱阳性表达,缺氧诱导48小时后c-myc蛋白表达显著升高（t=186.51,P〈0.05）,缺氧环境下As 203能抑制c-myc蛋白的表达（t=483.64,P〈0.05）.结论：缺氧环境下As 203能抑制c-myc蛋白的表达.     

Deregulation of c-myc and SV40Tag causing brain tumor in mice

Deregulated expressions of both c-myc and simian virus 40 large T antigen （SV40Tag） are consistent features of lots of tumors. To investigate whether the expression of c-myc and SV40Tag in mouse might help develop a model of human tumor, we generated c-myctransgenics by inserting human c-mycgene into pTRE2 of Tet-On system. We obtained conditional expression of SV4OTag transgenics by the Tet-On system from Yangzhou University. Crossing the c-myc transgenic mouse with the SV40Tag transgenic mice to generate bitransgenics we got double-transgenic mice expressing c-myc and SV40Tag by the Tet-On system. After being treated with doxycycline continuously, single-transgenic SV40Tag mice developed brain tumor infrequently （3 of 84, 3.6%） with a long onset （185 d on average）. In contrast, double-transgenic c-mydSV4OTag mice developed brain tumor with a short onset （96 days on average） and a 41% brain tumor incidence rate （7 of 17, 41%）. This tumor was assumed to be medulloblastoma. Our experiments suggest that deregulated expression of c-myc and SV4OTag in brain might generate a mouse model of human brain tumor that recapitulates some features of human medulloblastoma.     

Correlation of chromosomal polysomy with overexpression of c-myc and c-erbB-2 in primary nasopharyngeal carcinoma: Tissue microarray study

Many genes may be involved in nasopharyngeal carcinoma (NPC) development and progression. Several known oncogenes, including c-myc and c-erb-B2, have been shown to have structural alteration and aberrant expression in NPC. Here, we constructed a tissue microarray to determine the status of c-myc and c-erbB-2 oncogenes at the DNA and protein levels using interphase fluorescence in situ hybridization (FISH) and immunohistochemistry (IHC) and to define the diagnostic, prognostic importance of the genetic changes. Results showed that amplification of c-myc and c-erbB-2 was not found in NPC. Polysomy 8 and 17 were observed in 43%-50% and 20%-27% of NPC tumors, respectively. Overexpressions of c-myc and c-erbB-2 oncoproteins were detected in 53.6% and 54.5% cases of NPC with polysomy 8 and 17, respectively. There was no significant correlation between c-myc and c-erbB-2 staining and the clinical stage. But overexpression of c-erbB-2 was associated with polysomy 17 in NPC. These findings suggest that chromosomal polysomy, not gene amplification, may be partially responsible for the upregulated expression of c-erbB-2 oncogene in NPC.