基因失活
- 名gene inactivation
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结论:p53基因失活在脑肿瘤恶性进展过程中起重要作用。
Conclusion : p53 gene inactivation plays an important role in the malignant progression of brain tumors .
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卵巢癌PTEN基因失活机制的探讨
Research on the mechanisms of PTEN gene inactivation in ovarian cancer
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中国人群结、直肠癌p53基因失活突变热点的研究
A Study of Mutational Hot Spot of p53 Suppressor Gene in Chinese Colorectal Carcinoma
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P53基因失活与慢性粒细胞白血病的急变、病情进展密切相关。
The inactivation of P53 is associated with the acute transformation phase and development of CML .
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慢性炎症中持续的氧化应激导致DNA损伤并抑制损伤后修复。致使抑癌基因失活;
Sustained oxidative stress in the process of chronic inflammation leads to DNA damage and inhibition on its repair , resulting in inactivation of tumor suppressor genes .
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RNAi的机制是通过一段小片段双链RNA的作用序列特异性地使一段目的基因失活。
RNAi silences gene in a sequence-specific manner through the actions of small fragment of double-stranded RNAs .
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RNA干扰(RNAinterference,RNAi)是近年发展起来的一种特异的靶基因失活技术,它可以象基因敲除一样非常有效地鉴定特定基因的功能。
RNA interference ( RNAi ) is a gene-inactivating technologies that can efficiently identify the function of specific genes like gene knockout .
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引起外源基因失活的原因是多方面的,外源基因失活在DNA修饰水平,基因转录水平和转录后调节水平均可能发生。
There are many reasons that cause transgene inactivation , and inactivation can emerge at different gene expression stage , such as DNA modification level , transcriptional level and post-transcriptional level .
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RNAi已成为一种极为有用的使基因失活的工具应用于多方面的研究中。
RNAi has become a tool to inactivate gene and has been applied in many researches .
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膀胱癌细胞p16抑癌基因失活的研究
Inactivation of the p16 / MTSI gene in bladder cancer
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卵巢癌PTEN基因失活和细胞外信号调节激酶的活化机制以及与卵巢癌耐药的关系
The Relation between Mechanisms of PTEN Gene Inactivation and the Activation of Extracellular Signal-regulated Kinase and Drug Resistance in Ovarian Cancer
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p53基因失活、HIF-1α、VEGF过表达及高MVD与结直肠癌的不良生物学行为有关。
Loss of p53 function , overexpression of HIF-1 α and VEGF and higher MVD are related with the poor biological behavior of colorectal carcinoma .
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近年来,DNA启动子甲基化作为抑癌基因失活的一条重要途径,在肿瘤发生发展中起着关键的作用,成为国内外研究的热点。
As one of the most important way of the tumor-suppressor gene inactivation , the methylation of gene promoter plays a key role in the development of tumor . In recent years , it has become the research focus .
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其中,CpG岛的异常高甲基化使得一些关键的抑癌基因失活是引发癌症的重要机制。
In which , the abnormal methylation of CpG island methylation that makes some tumor suppressor gene inactivation is the key to cancer .
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人类肿瘤p16~(INK4a)/CDKN2A基因失活机制及应用
Mechanisms and Significance of the p16 ~ ( INK4a ) / CDKN2A Gene Alterations in Human Tumors
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它们分别与细胞凋亡、癌基因失活、血管生成、转录调控及信号转导等有关,并对其中的6个差异蛋白在mRNA和蛋白质水平进行了验证。
These differential proteins are related to cell apoptosis , angiogenesis , oncogene inactivation , transcriptional control and signal transduction , etc. RT-PCR and western blot were employed to verify 6 differential proteins on the mRNA and protein levels .
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角质形成细胞增生行为与p16~(INK4a)蛋白表达和基因失活的相关性研究
Correlation study between proliferative behavior of human keratinocyte and p16 ~ ( INK4a ) protein expression and gene inactivation
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结论HIF-1α/VEGF通路在结直肠癌组织血管生成过程中起重要作用,p53基因失活可能经HIF-1α/VEGF通路促进肿瘤血管生成。
Conclusions : HIF-1 α / VEGF pathway may play an important role in angiogenesis of colorectal carcinoma . Loss of p53 function may facilitate angiogenesis via HIF-1 α / VEGF pathway .
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P53基因失活和突变能降低血管生成阻止因子的分泌从而激发VEGF在肿瘤中的表达,促使乳腺癌的发生发展和转移。
Deletion and mutation of P53 gene can decrease secretion of angiogenesis inhibitor and induce expression of VEGF in breast cancer . Deletion and mutation of P53 gene also play a role in the progression and metastasis in breast cancer .
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对此片段测序后进行生物信息学分析表明:其结构中含有与转座和同源重组有关的成分,提示了部分肿瘤细胞中p16~(INK4a)基因失活的可能原因。
Bioinformatics analysis suggests that the structure of this DNA fragment may be responsible for the p16 ~ ( INK4a ) inactivation found in some tumors .
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结论多于半数的HNPCC发生APC突变,其突变多发生在编码区单核苷酸重复序列(移码突变)或CpG岛(点突变)上,提示APC基因失活在HNPCC为常见的分子事件;
Conclusion Mutational inactivations of APC gene were detected in more than half of HNPCC patients in this study , indicating that APC mutation is a common molecular event in the tumorigenesis of HNPCC .
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既往认为抑癌基因失活有两条途径:基因内突变和染色体物质丢失(杂合性丢失LOH或等位基因丢失)。
It was thought formerly that two pathways by which tumor suppressor genes became disabled were intragenic mutations and loss of chromosomal material [ ( loss of heterozygosity ( LOH ) or homozygous deletion ) ] .
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上述结果表明,A1412突变体表型的改变可能是由于TDNA插入而使某一具有重要生物学功能的基因失活所致。
These data suggest that an important biological process blocked in A1-412 was likely to be due to the insertion of T-DNA and the subsequent disruption of gene function .
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上皮源性恶性肿瘤患者p16/MTS1抑癌基因失活研究
Inactivation of the p16 / MTS1 Gene in Multiple Human Cancers
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子宫内膜癌p16/MTS1基因失活的研究
Study on p16 / MTS1 gene inactivation in carcinoma of endometrium
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葡聚糖结合蛋白D基因失活影响变形链球菌生物膜的形成
Inactivation of glucan-binding protein D gene affects the biofilm formation by Streptococcus mutatis
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抑癌基因失活在多原发性恶性肿瘤发生中的意义
The significance of tumor supressor genes inactivation in carcinogenesis of multiple primary neoplasm
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中国儿童白血病中P~(53)基因失活突变的研究
Mutations of the P  ̄( 53 ) Gene in Chinese Children with Leukemia
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肝细胞癌多种抑癌基因失活机理的研究
Studies on the mechanism of inactivation of multiple tumour suppressor genes in hepatocellular carcinoma
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这种染色体异常使控制细胞生长的关键肿瘤抑制基因失活。
Such chromosomal abnormalities inactivate tumor-suppressor genes that are critical for controlling cell growth .